Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.
Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.
Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.
The application of repeated, brief periods of vascular occlusion at the onset of REPERFUSION to reduce REPERFUSION INJURY that follows a prolonged ischemic event. The techniques are similar to ISCHEMIC PRECONDITIONING but the time of application is after the ischemic event instead of before.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.
Solutions which, upon administration, will temporarily arrest cardiac activity. They are used in the performance of heart surgery.
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).
The circulation of blood through the CORONARY VESSELS of the HEART.
A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7.
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing REPERFUSION INJURY.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
The hollow, muscular organ that maintains the circulation of the blood.
A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Contractile activity of the MYOCARDIUM.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
Surgical removal of an obstructing clot or foreign material from a blood vessel at the point of its formation. Removal of a clot arising from a distant site is called EMBOLECTOMY.
Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.
Exposure of myocardial tissue to brief, repeated periods of vascular occlusion in order to render the myocardium resistant to the deleterious effects of ISCHEMIA or REPERFUSION. The period of pre-exposure and the number of times the tissue is exposed to ischemia and reperfusion vary, the average being 3 to 5 minutes.
The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure.
Elements of limited time intervals, contributing to particular results or situations.
Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.
A technique in which tissue is rendered resistant to the deleterious effects of prolonged ISCHEMIA and REPERFUSION by prior exposure to brief, repeated periods of vascular occlusion. (Am J Physiol 1995 May;268(5 Pt 2):H2063-7, Abstract)
The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.
Treatment process involving the injection of fluid into an organ or tissue.
A procedure to stop the contraction of MYOCARDIUM during HEART SURGERY. It is usually achieved with the use of chemicals (CARDIOPLEGIC SOLUTIONS) or cold temperature (such as chilled perfusate).
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
The veins and arteries of the HEART.
Radiography of the vascular system of the heart muscle after injection of a contrast medium.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.
An isoenzyme of creatine kinase found in the CARDIAC MUSCLE.
The mitochondria of the myocardium.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
MYOCARDIAL INFARCTION in which the anterior wall of the heart is involved. Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. It can be categorized as anteroseptal or anterolateral wall myocardial infarction.
Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
A family of percutaneous techniques that are used to manage CORONARY OCCLUSION, including standard balloon angioplasty (PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY), the placement of intracoronary STENTS, and atheroablative technologies (e.g., ATHERECTOMY; ENDARTERECTOMY; THROMBECTOMY; PERCUTANEOUS TRANSLUMINAL LASER ANGIOPLASTY). PTCA was the dominant form of PCI, before the widespread use of stenting.
Injuries incurred during participation in competitive or non-competitive sports.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).
The dialdehyde of malonic acid.
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
A tissue or organ remaining at physiological temperature during decreased BLOOD perfusion or in the absence of blood supply. During ORGAN TRANSPLANTATION it begins when the organ reaches physiological temperature before the completion of SURGICAL ANASTOMOSIS and ends with reestablishment of the BLOOD CIRCULATION through the tissue.
Damage to any compartment of the lung caused by physical, chemical, or biological agents which characteristically elicit inflammatory reaction. These inflammatory reactions can either be acute and dominated by NEUTROPHILS, or chronic and dominated by LYMPHOCYTES and MACROPHAGES.
Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
An anatomic severity scale based on the Abbreviated Injury Scale (AIS) and developed specifically to score multiple traumatic injuries. It has been used as a predictor of mortality.
The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
General or unspecified injuries involving the leg.
The chilling of a tissue or organ during decreased BLOOD perfusion or in the absence of blood supply. Cold ischemia time during ORGAN TRANSPLANTATION begins when the organ is cooled with a cold perfusion solution after ORGAN PROCUREMENT surgery, and ends after the tissue reaches physiological temperature during implantation procedures.
The process by which organs are kept viable outside of the organism from which they were removed (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The process by which chemical compounds provide protection to cells against harmful agents.
Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.
A condition of lung damage that is characterized by bilateral pulmonary infiltrates (PULMONARY EDEMA) rich in NEUTROPHILS, and in the absence of clinical HEART FAILURE. This can represent a spectrum of pulmonary lesions, endothelial and epithelial, due to numerous factors (physical, chemical, or biological).
An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1.
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC 2.6.1.2.
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC 2.6.1.1.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and intraocular injuries.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated.
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
General or unspecified injuries to the neck. It includes injuries to the skin, muscles, and other soft tissues of the neck.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
Substances that influence the course of a chemical reaction by ready combination with free radicals. Among other effects, this combining activity protects pancreatic islets against damage by cytokines and prevents myocardial and pulmonary perfusion injuries.
Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
The act of constricting.
Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.
In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.

Differential regulation of Bcl-2, AP-1 and NF-kappaB on cardiomyocyte apoptosis during myocardial ischemic stress adaptation. (1/3052)

Acute ischemia followed by prolonged reperfusion has been shown to induce cardiomyocyte apoptosis. In this report, we demonstrate that myocardial adaptation to ischemia induced by repeated cyclic episodes of short-term ischemia each followed by another short duration of reperfusion reduced cardiomyocyte apoptosis and DNA fragmentation. This was associated with the induction of the expression of Bcl-2 mRNA and translocation and activation of NF-kappaB. Another transcription factor, AP-1, remained unaffected by repeated ischemia and reperfusion, but exhibited significant upregulation by a single episode of 30 min ischemia followed by 2 h of reperfusion. This activation of AP-1 was inhibited by a scavenger of oxygen free radicals, DMTU. Thirty minutes ischemia and 120 min reperfusion downregulated the induction of the expression of Bcl-2 mRNA, but moderately activated NF-kappaB binding activity. This was associated with an increased number of apoptotic cells and DNA fragmentation in cardiomyocytes which were attenuated by DMTU. The results of this study indicate that Bcl-2, AP-1 and NF-kappaB differentially regulate cardiomyocyte apoptosis mediated by acute ischemia and prolonged reperfusion.  (+info)

Reactive oxygen species play an important role in the activation of heat shock factor 1 in ischemic-reperfused heart. (2/3052)

BACKGROUND: The myocardial protective role of heat shock protein (HSP) has been demonstrated. Recently, we reported that ischemia/reperfusion induced a significant activation of heat shock factor (HSF) 1 and an accumulation of mRNA for HSP70 and HSP90. We examined the role of reactive oxygen species (ROSs) in the induction of stress response in the ischemic-reperfused heart. METHODS AND RESULTS: Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element. Induction of mRNA for HSP70 and HSP90 was examined by Northern blot analysis. Repetitive ischemia/reperfusion, which causes recurrent bursts of free radical generation, resulted in burst activation of HSF1, and this burst activation was significantly reduced with either allopurinol 1 mmol/L (an inhibitor of xanthine oxidase) or catalase 2x10(5) U/L (a scavenger of H2O2). Significant activation of HSF1 was observed on perfusion with buffer containing H2O2 150 micromol/L or xanthine 1 mmol/L plus xanthine oxidase 5 U/L. The accumulation of mRNA for HSP70 or HSP90 after repetitive ischemia/reperfusion was reduced with either allopurinol or catalase. CONCLUSIONS: Our findings demonstrate that ROSs play an important role in the activation of HSF1 and the accumulation of mRNA for HSP70 and HSP90 in the ischemic-reperfused heart.  (+info)

Nonanticoagulant heparin prevents coronary endothelial dysfunction after brief ischemia-reperfusion injury in the dog. (3/3052)

BACKGROUND: Coronary endothelial dysfunction after brief ischemia-reperfusion (IR) remains a clinical problem. We investigated the role of heparin and N-acetylheparin, a nonanticoagulant heparin derivative, in modulating coronary endothelial function after IR injury, with an emphasis on defining the role of the nitric oxide (NO)-cGMP pathway in the heparin-mediated effect. METHODS AND RESULTS: Male mongrel dogs were surgically instrumented, and the effects of both bovine heparin and N-acetylheparin on coronary endothelial vasomotor function, expressed as percent change from baseline flow after acetylcholine challenge, were studied after 15 minutes of regional ischemia of the left anterior descending artery (LAD) followed by 120 minutes of reperfusion. In dogs treated with placebo (saline), coronary vasomotor function was significantly (P+info)

Tumor necrosis factor-alpha contributes to ischemia- and reperfusion-induced endothelial activation in isolated hearts. (4/3052)

-During myocardial reperfusion, polymorphonuclear neutrophil (PMN) adhesion involving the intercellular adhesion molecule-1 (ICAM-1) may lead to aggravation and prolongation of reperfusion injury. We studied the role of early tumor necrosis factor-alpha (TNF-alpha) cleavage and nuclear factor-kappaB (NF-kappaB) activation on ICAM-1 expression and venular adhesion of PMN in isolated hearts after ischemia (15 minutes) and reperfusion (30 to 480 minutes). NF-kappaB activation (electromobility shift assay) was found after 30 minutes of reperfusion and up to 240 minutes. ICAM-1 mRNA, assessed by Northern blot, increased during the same interval. Functional effect of newly synthesized adhesion molecules was found by quantification (in situ fluorescence microscopy) of PMN, given as bolus after ischemia, which became adherent to small coronary venules (10 to 50 microm in diameter). After 480 minutes of reperfusion, ICAM-1-dependent PMN adhesion increased 2.5-fold compared with PMN adhesion obtained during acute reperfusion. To study the influence of NF-kappaB on PMN adhesion, we inhibited NF-kappaB activation by transfection of NF-kappaB decoy oligonucleotides into isolated hearts using HJV-liposomes. Decoy NF-kappaB but not control oligonucleotides blocked ICAM-1 upregulation and inhibited the subacute increase in PMN adhesion. Similar effects were obtained using BB 1101 (10 microg), an inhibitor of TNF-alpha cleavage enzyme. These data suggest that ischemia and reperfusion in isolated hearts cause liberation of TNF-alpha, activation of NF-kappaB, and upregulation of ICAM-1, an adhesion molecule involved in inflammatory response after ischemia and reperfusion.  (+info)

Effects of isoproterenol on myocardial structure and function in septic rats. (5/3052)

In this study we sought to determine the effect of sepsis on two sequelae of prolonged (24-h) beta-agonist administration, myocardial hypertrophy and catecholamine-induced cardiotoxicity. Sprague-Dawley rats were randomized to cecal ligation and perforation (CLP) or sham study groups and then further randomized to receive isoproterenol (2.4 mg. kg-1. day-1 iv) or placebo treatment. At 24 h, myocardial function was assessed by using the Langendorff isolated-heart technique or the heart processed for plain light microscopy. We found that 1) sepsis reduced contractile function, indicated by a rightward shift in the Starling curve (ANOVA with repeated measures, sepsis effect, P < 0.002); 2) sepsis-induced myocardial depression was reversed by isoproterenol treatment (isoproterenol effect, P < 0.0001); 3) sepsis reduced, but did not block, isoproterenol-induced myocardial hypertrophy (isoproterenol effect, P < 0.0001); 4) sepsis did not protect the heart from catecholamine-induced tissue injury; 5) the septic heart was protected against the effects of ischemiareperfusion (decreased postreperfusion resting tension, ANOVA with repeated measures, P < 0.01), an effect attenuated by isoproterenol treatment (P < 0.005); and 6) sepsis reduced the incidence of sustained asystole or ventricular fibrillation after ischemia-reperfusion (P < 0.05), an effect also attenuated by isoproterenol treatment (P < 0.01). We conclude that, in sepsis, beta-agonists induce changes in myocardial weight and function consistent with acute myocardial hypertrophy. These changes occur at the expense of significant tissue injury and increased sensitivity to ischemia-reperfusion-induced tissue injury.  (+info)

Formation of 4-hydroxy-2-nonenal-modified proteins in ischemic rat heart. (6/3052)

4-Hydroxy-2-nonenal (HNE) is a major lipid peroxidation product formed during oxidative stress. Because of its reactivity with nucleophilic compounds, particularly metabolites and proteins containing thiol groups, HNE is cytotoxic. The aim of this study was to assess the extent and time course for the formation of HNE-modified proteins during ischemia and ischemia plus reperfusion in isolated rat hearts. With an antibody to HNE-Cys/His/Lys and densitometry of Western blots, we quantified the amount of HNE-protein adduct in the heart. By taking biopsies from single hearts (n = 5) at various times (0, 5, 10, 15, 20, 35, and 40 min) after onset of zero-flow global ischemia, we showed a progressive, time-dependent increase (which peaked after 30 min) in HNE-mediated modification of a discrete number of proteins. In studies with individual hearts (n = 4/group), control aerobic perfusion (70 min) resulted in a very low level (296 arbitrary units) of HNE-protein adduct formation; by contrast, after 30-min ischemia HNE-adduct content increased by >50-fold (15,356 units, P < 0.05). In other studies (n = 4/group), administration of N-(2-mercaptopropionyl)glycine (MPG, 1 mM) to the heart for 5 min immediately before 30-min ischemia reduced HNE-protein adduct formation during ischemia by approximately 75%. In studies (n = 4/group) that included reperfusion of hearts after 5, 10, 15, or 30 min of ischemia, there was no further increase in the extent of HNE-protein adduct formation over that seen with ischemia alone. Similarly, in experiments with MPG, reperfusion did not significantly influence the tissue content of HNE-protein adduct. Western immunoblot results were confirmed in studies using in situ immunofluorescent localization of HNE-protein in cryosections. In conclusion, ischemia causes a major increase in HNE-protein adduct that would be expected to reflect a toxic sequence of events that might act to compromise tissue survival during ischemia and recovery on reperfusion.  (+info)

Metallothionein inhibits ischemia-reperfusion injury in mouse heart. (7/3052)

Oxidative stress is believed to play a major role in ischemia-reperfusion injury to the heart. Metallothionein (MT), a potential free radical scavenger, may function in cardiac protection against ischemia-reperfusion damage. To test this hypothesis, a specific cardiac MT-overexpressing transgenic mouse model was used. The hearts isolated from these animals were subjected to 50 min of warm (37 degrees C) zero-flow ischemia followed by 60- or 90-min reflow. Compared with the nontransgenic controls, the transgenic mouse hearts with MT concentrations approximately 10-fold higher than normal showed significantly improved recovery of contractile force postischemia (69.2 +/- 4.2 vs. 26.0 +/- 6.0% at the end of 60-min reperfusion, P < 0.01). Efflux of creatine kinase from these transgenic hearts was reduced by more than 50% (P < 0.01). In addition, the zone of infarction induced by ischemia-reperfusion at the end of 90-min reperfusion was suppressed by approximately 40% (P < 0.01) in the transgenic hearts. The results strongly indicate that MT provides protection against ischemia-reperfusion-induced heart injury.  (+info)

Acute exercise can improve cardioprotection without increasing heat shock protein content. (8/3052)

The aim of this study was to determine the effects of acute bouts of exercise on myocardial recovery after ischemia and heat shock protein expression. Adult female Sprague-Dawley rats were divided into five groups: 1) 1-day run (1DR; n = 6) and 2) 3-day run (3DR; n = 7), in which rats ran for 100 min at a speed of 20 m/min up a 6 degrees grade for 1 or 3 consecutive days; 3) 1-day cold run (1CR), in which rats ran the same as 1DR but with wet fur at 8 degrees C, which prevented an elevation of core temperature (n = 8); 4) heat shock sedentary (HS), in which rats had their core temperatures raised to 42 degrees C one time for 15 min (n = 5); and 5) sedentary control (n=15). Cardiac function was analyzed 24 h after the last treatment using an isolated, working heart model. Nonpaced hearts were initially perfused under normoxic conditions, then underwent 17 min of global, normothermic (37 degrees C) ischemia, and, finally, were allowed to recover for 30 min under normoxic conditions. The concentration of the 72-kDa heat shock protein (HSP 72) was measured in each left ventricle. Compared with that in the sedentary group, recovery of cardiac output x systolic pressure (CO x SP) was enhanced (P < 0.05) in all treatment groups when the postischemic value was covaried with the preischemic value. No differences in CO x SP were found (P > 0.05) between the following groups: 1DR vs. 3DR, 1DR vs. HS, and 1DR vs. 1CR. Heat shock protein concentration was significantly greater (P < 0.05) than that in the sedentary controls in HS, 1DR, and 3DR groups, but not for 1CR. The concentration of HSP 72 was not significantly correlated with postischemic CO x SP (R2 = 0.197, P > 0.05). We conclude that acute bouts of exercise can produce cardioprotective effects without an elevation of HSP 72.  (+info)

Myocardial reperfusion injury is a pathological process that occurs when blood flow is restored to the heart muscle (myocardium) after a period of ischemia or reduced oxygen supply, such as during a myocardial infarction (heart attack). The restoration of blood flow, although necessary to salvage the dying tissue, can itself cause further damage to the heart muscle. This paradoxical phenomenon is known as myocardial reperfusion injury.

The mechanisms behind myocardial reperfusion injury are complex and involve several processes, including:

1. Oxidative stress: The sudden influx of oxygen into the previously ischemic tissue leads to an overproduction of reactive oxygen species (ROS), which can damage cellular structures, such as proteins, lipids, and DNA.
2. Calcium overload: During reperfusion, there is an increase in calcium influx into the cardiomyocytes (heart muscle cells). This elevated intracellular calcium level can disrupt normal cellular functions, leading to further damage.
3. Inflammation: Reperfusion triggers an immune response, with the recruitment of inflammatory cells, such as neutrophils and monocytes, to the site of injury. These cells release cytokines and other mediators that can exacerbate tissue damage.
4. Mitochondrial dysfunction: The restoration of blood flow can cause mitochondria, the powerhouses of the cell, to malfunction, leading to the release of pro-apoptotic factors and contributing to cell death.
5. Vasoconstriction and microvascular obstruction: During reperfusion, there may be vasoconstriction of the small blood vessels (microvasculature) in the heart, which can further limit blood flow and contribute to tissue damage.

Myocardial reperfusion injury is a significant concern because it can negate some of the benefits of early reperfusion therapy, such as thrombolysis or primary percutaneous coronary intervention (PCI), used to treat acute myocardial infarction. Strategies to minimize myocardial reperfusion injury are an area of active research and include pharmacological interventions, ischemic preconditioning, and remote ischemic conditioning.

Myocardial reperfusion is the restoration of blood flow to the heart muscle (myocardium), usually after a period of ischemia or reduced oxygen supply, such as during a myocardial infarction (heart attack). This can be achieved through various medical interventions, including thrombolytic therapy, percutaneous coronary intervention (PCI), or coronary artery bypass surgery (CABG). The goal of myocardial reperfusion is to salvage the jeopardized myocardium, preserve cardiac function, and reduce the risk of complications like heart failure or arrhythmias. However, it's important to note that while reperfusion is crucial for treating ischemic heart disease, it can also lead to additional injury to the heart muscle, known as reperfusion injury.

Reperfusion injury is a complex pathophysiological process that occurs when blood flow is restored to previously ischemic tissues, leading to further tissue damage. This phenomenon can occur in various clinical settings such as myocardial infarction (heart attack), stroke, or peripheral artery disease after an intervention aimed at restoring perfusion.

The restoration of blood flow leads to the generation of reactive oxygen species (ROS) and inflammatory mediators, which can cause oxidative stress, cellular damage, and activation of the immune system. This results in a cascade of events that may lead to microvascular dysfunction, capillary leakage, and tissue edema, further exacerbating the injury.

Reperfusion injury is an important consideration in the management of ischemic events, as interventions aimed at restoring blood flow must be carefully balanced with potential harm from reperfusion injury. Strategies to mitigate reperfusion injury include ischemic preconditioning (exposing the tissue to short periods of ischemia before a prolonged ischemic event), ischemic postconditioning (applying brief periods of ischemia and reperfusion after restoring blood flow), remote ischemic preconditioning (ischemia applied to a distant organ or tissue to protect the target organ), and pharmacological interventions that scavenge ROS, reduce inflammation, or improve microvascular function.

Ischemic postconditioning is a medical/physiological term that refers to a cardioprotective strategy used to mitigate the damage caused by ischemia-reperfusion injury, which occurs during myocardial infarction (heart attack) or other conditions involving restricted blood flow to the heart muscle.

The technique involves applying brief, intermittent periods of reduced blood flow (ischemia) and reflow (reperfusion) to the heart immediately after a prolonged period of ischemia. This process triggers a complex intracellular signaling cascade that helps protect the heart tissue from further damage during reperfusion.

The protective effects of ischemic postconditioning are attributed to various cellular and molecular mechanisms, such as reducing oxidative stress, inhibiting inflammation, preserving mitochondrial function, and modulating calcium homeostasis. These combined actions help minimize the infarct size (area of damaged heart tissue) and improve overall cardiac function following an ischemic event.

Ischemic postconditioning has been explored as a potential therapeutic approach to treat ischemia-reperfusion injuries in various clinical settings, including heart attacks, cardiac surgery, and organ transplantation. However, its translation into clinical practice has been challenging due to the complexity of the intervention and the need for precise timing and control over the ischemic and reperfusion periods.

Myocardial infarction (MI), also known as a heart attack, is a medical condition characterized by the death of a segment of heart muscle (myocardium) due to the interruption of its blood supply. This interruption is most commonly caused by the blockage of a coronary artery by a blood clot formed on the top of an atherosclerotic plaque, which is a buildup of cholesterol and other substances in the inner lining of the artery.

The lack of oxygen and nutrients supply to the heart muscle tissue results in damage or death of the cardiac cells, causing the affected area to become necrotic. The extent and severity of the MI depend on the size of the affected area, the duration of the occlusion, and the presence of collateral circulation.

Symptoms of a myocardial infarction may include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and sweating. Immediate medical attention is necessary to restore blood flow to the affected area and prevent further damage to the heart muscle. Treatment options for MI include medications, such as thrombolytics, antiplatelet agents, and pain relievers, as well as procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

Creatine kinase (CK) is a muscle enzyme that is normally present in small amounts in the blood. It is primarily found in tissues that require a lot of energy, such as the heart, brain, and skeletal muscles. When these tissues are damaged or injured, CK is released into the bloodstream, causing the levels to rise.

Creatine kinase exists in several forms, known as isoenzymes, which can be measured in the blood to help identify the location of tissue damage. The three main isoenzymes are:

1. CK-MM: Found primarily in skeletal muscle
2. CK-MB: Found primarily in heart muscle
3. CK-BB: Found primarily in the brain

Elevated levels of creatine kinase, particularly CK-MB, can indicate damage to the heart muscle, such as occurs with a heart attack. Similarly, elevated levels of CK-BB may suggest brain injury or disease. Overall, measuring creatine kinase levels is a useful diagnostic tool for assessing tissue damage and determining the severity of injuries or illnesses.

Cardioplegic solutions are specially formulated liquids used in medical procedures to induce cardiac arrest and protect the heart muscle during open-heart surgery. These solutions typically contain a combination of electrolytes, such as potassium and magnesium, which stop the heart from beating by interrupting its electrical activity. They may also include energy substrates, buffers, and other components to maintain the health and function of the heart cells during the period of arrest. The specific formulation of cardioplegic solutions can vary depending on the needs of the patient and the preferences of the medical team.

Myocardial ischemia is a condition in which the blood supply to the heart muscle (myocardium) is reduced or blocked, leading to insufficient oxygen delivery and potential damage to the heart tissue. This reduction in blood flow typically results from the buildup of fatty deposits, called plaques, in the coronary arteries that supply the heart with oxygen-rich blood. The plaques can rupture or become unstable, causing the formation of blood clots that obstruct the artery and limit blood flow.

Myocardial ischemia may manifest as chest pain (angina pectoris), shortness of breath, fatigue, or irregular heartbeats (arrhythmias). In severe cases, it can lead to myocardial infarction (heart attack) if the oxygen supply is significantly reduced or cut off completely, causing permanent damage or death of the heart muscle. Early diagnosis and treatment of myocardial ischemia are crucial for preventing further complications and improving patient outcomes.

Coronary circulation refers to the circulation of blood in the coronary vessels, which supply oxygenated blood to the heart muscle (myocardium) and drain deoxygenated blood from it. The coronary circulation system includes two main coronary arteries - the left main coronary artery and the right coronary artery - that branch off from the aorta just above the aortic valve. These arteries further divide into smaller branches, which supply blood to different regions of the heart muscle.

The left main coronary artery divides into two branches: the left anterior descending (LAD) artery and the left circumflex (LCx) artery. The LAD supplies blood to the front and sides of the heart, while the LCx supplies blood to the back and sides of the heart. The right coronary artery supplies blood to the lower part of the heart, including the right ventricle and the bottom portion of the left ventricle.

The veins that drain the heart muscle include the great cardiac vein, the middle cardiac vein, and the small cardiac vein, which merge to form the coronary sinus. The coronary sinus empties into the right atrium, allowing deoxygenated blood to enter the right side of the heart and be pumped to the lungs for oxygenation.

Coronary circulation is essential for maintaining the health and function of the heart muscle, as it provides the necessary oxygen and nutrients required for proper contraction and relaxation of the myocardium. Any disruption or blockage in the coronary circulation system can lead to serious consequences, such as angina, heart attack, or even death.

Peroxidase is a type of enzyme that catalyzes the chemical reaction in which hydrogen peroxide (H2O2) is broken down into water (H2O) and oxygen (O2). This enzymatic reaction also involves the oxidation of various organic and inorganic compounds, which can serve as electron donors.

Peroxidases are widely distributed in nature and can be found in various organisms, including bacteria, fungi, plants, and animals. They play important roles in various biological processes, such as defense against oxidative stress, breakdown of toxic substances, and participation in metabolic pathways.

The peroxidase-catalyzed reaction can be represented by the following chemical equation:

H2O2 + 2e- + 2H+ → 2H2O

In this reaction, hydrogen peroxide is reduced to water, and the electron donor is oxidized. The peroxidase enzyme facilitates the transfer of electrons between the substrate (hydrogen peroxide) and the electron donor, making the reaction more efficient and specific.

Peroxidases have various applications in medicine, industry, and research. For example, they can be used for diagnostic purposes, as biosensors, and in the treatment of wastewater and medical wastes. Additionally, peroxidases are involved in several pathological conditions, such as inflammation, cancer, and neurodegenerative diseases, making them potential targets for therapeutic interventions.

Cardiotonic agents are a type of medication that have a positive inotropic effect on the heart, meaning they help to improve the contractility and strength of heart muscle contractions. These medications are often used to treat heart failure, as they can help to improve the efficiency of the heart's pumping ability and increase cardiac output.

Cardiotonic agents work by increasing the levels of calcium ions inside heart muscle cells during each heartbeat, which in turn enhances the force of contraction. Some common examples of cardiotonic agents include digitalis glycosides (such as digoxin), which are derived from the foxglove plant, and synthetic medications such as dobutamine and milrinone.

While cardiotonic agents can be effective in improving heart function, they can also have potentially serious side effects, including arrhythmias, electrolyte imbalances, and digestive symptoms. As a result, they are typically used under close medical supervision and their dosages may need to be carefully monitored to minimize the risk of adverse effects.

Reperfusion, in medical terms, refers to the restoration of blood flow to tissues or organs that have been deprived of adequate oxygen supply, usually as a result of ischemia (lack of blood flow). This process is often initiated through therapeutic interventions such as thrombolysis (breaking up blood clots), angioplasty (opening narrowed or blocked blood vessels using a balloon or stent), or surgical procedures.

Reperfusion aims to salvage the affected tissues and prevent further damage; however, it can also lead to reperfusion injury. This injury occurs when the return of oxygen-rich blood to previously ischemic tissues results in the overproduction of free radicals and inflammatory mediators, which can cause additional cellular damage and organ dysfunction.

Managing reperfusion injury involves using various strategies such as antioxidants, anti-inflammatory agents, and other protective treatments to minimize its negative impact on the recovering tissues or organs.

P-Selectin is a type of cell adhesion molecule, specifically a member of the selectin family, that is involved in the inflammatory response. It is primarily expressed on the surface of activated platelets and endothelial cells. P-Selectin plays a crucial role in the initial interaction between leukocytes (white blood cells) and the vascular endothelium, which is an essential step in the recruitment of leukocytes to sites of inflammation or injury. This process helps to mediate the rolling and adhesion of leukocytes to the endothelial surface, facilitating their extravasation into the surrounding tissue. P-Selectin's function is regulated by its interaction with specific ligands on the surface of leukocytes, such as PSGL-1 (P-Selectin Glycoprotein Ligand-1).

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Hemodynamics is the study of how blood flows through the cardiovascular system, including the heart and the vascular network. It examines various factors that affect blood flow, such as blood volume, viscosity, vessel length and diameter, and pressure differences between different parts of the circulatory system. Hemodynamics also considers the impact of various physiological and pathological conditions on these variables, and how they in turn influence the function of vital organs and systems in the body. It is a critical area of study in fields such as cardiology, anesthesiology, and critical care medicine.

In medical terms, the heart is a muscular organ located in the thoracic cavity that functions as a pump to circulate blood throughout the body. It's responsible for delivering oxygen and nutrients to the tissues and removing carbon dioxide and other wastes. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it out to the rest of the body. The heart's rhythmic contractions and relaxations are regulated by a complex electrical conduction system.

"Random allocation," also known as "random assignment" or "randomization," is a process used in clinical trials and other research studies to distribute participants into different intervention groups (such as experimental group vs. control group) in a way that minimizes selection bias and ensures the groups are comparable at the start of the study.

In random allocation, each participant has an equal chance of being assigned to any group, and the assignment is typically made using a computer-generated randomization schedule or other objective methods. This process helps to ensure that any differences between the groups are due to the intervention being tested rather than pre-existing differences in the participants' characteristics.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

I believe there might be a misunderstanding in your question. "Dogs" is not a medical term or condition. It is the common name for a domesticated carnivore of the family Canidae, specifically the genus Canis, which includes wolves, foxes, and other extant and extinct species of mammals. Dogs are often kept as pets and companions, and they have been bred in a wide variety of forms and sizes for different purposes, such as hunting, herding, guarding, assisting police and military forces, and providing companionship and emotional support.

If you meant to ask about a specific medical condition or term related to dogs, please provide more context so I can give you an accurate answer.

Myocardial contraction refers to the rhythmic and forceful shortening of heart muscle cells (myocytes) in the myocardium, which is the muscular wall of the heart. This process is initiated by electrical signals generated by the sinoatrial node, causing a wave of depolarization that spreads throughout the heart.

During myocardial contraction, calcium ions flow into the myocytes, triggering the interaction between actin and myosin filaments, which are the contractile proteins in the muscle cells. This interaction causes the myofilaments to slide past each other, resulting in the shortening of the sarcomeres (the functional units of muscle contraction) and ultimately leading to the contraction of the heart muscle.

Myocardial contraction is essential for pumping blood throughout the body and maintaining adequate circulation to vital organs. Any impairment in myocardial contractility can lead to various cardiac disorders, such as heart failure, cardiomyopathy, and arrhythmias.

Neutrophils are a type of white blood cell that are part of the immune system's response to infection. They are produced in the bone marrow and released into the bloodstream where they circulate and are able to move quickly to sites of infection or inflammation in the body. Neutrophils are capable of engulfing and destroying bacteria, viruses, and other foreign substances through a process called phagocytosis. They are also involved in the release of inflammatory mediators, which can contribute to tissue damage in some cases. Neutrophils are characterized by the presence of granules in their cytoplasm, which contain enzymes and other proteins that help them carry out their immune functions.

A thrombectomy is a medical procedure that involves the removal of a blood clot (thrombus) from a blood vessel. This is typically performed to restore blood flow in cases where the clot is causing significant blockage, which can lead to serious complications such as tissue damage or organ dysfunction.

During a thrombectomy, a surgeon makes an incision and accesses the affected blood vessel, often with the help of imaging guidance. Specialized tools are then used to extract the clot, after which the blood vessel is usually repaired. Thrombectomies can be performed on various blood vessels throughout the body, including those in the brain, heart, lungs, and limbs.

This procedure may be recommended for patients with deep vein thrombosis (DVT), pulmonary embolism (PE), or certain types of stroke, depending on the specific circumstances and the patient's overall health. It is generally considered when anticoagulation therapy or clot-dissolving medications are not sufficient or appropriate to treat the blood clot.

A wound is a type of injury that occurs when the skin or other tissues are cut, pierced, torn, or otherwise broken. Wounds can be caused by a variety of factors, including accidents, violence, surgery, or certain medical conditions. There are several different types of wounds, including:

* Incisions: These are cuts that are made deliberately, often during surgery. They are usually straight and clean.
* Lacerations: These are tears in the skin or other tissues. They can be irregular and jagged.
* Abrasions: These occur when the top layer of skin is scraped off. They may look like a bruise or a scab.
* Punctures: These are wounds that are caused by sharp objects, such as needles or knives. They are usually small and deep.
* Avulsions: These occur when tissue is forcibly torn away from the body. They can be very serious and require immediate medical attention.

Injuries refer to any harm or damage to the body, including wounds. Injuries can range from minor scrapes and bruises to more severe injuries such as fractures, dislocations, and head trauma. It is important to seek medical attention for any injury that is causing significant pain, swelling, or bleeding, or if there is a suspected bone fracture or head injury.

In general, wounds and injuries should be cleaned and covered with a sterile bandage to prevent infection. Depending on the severity of the wound or injury, additional medical treatment may be necessary. This may include stitches for deep cuts, immobilization for broken bones, or surgery for more serious injuries. It is important to follow your healthcare provider's instructions carefully to ensure proper healing and to prevent complications.

Ischemic preconditioning, myocardial is a phenomenon in cardiac physiology where the heart muscle (myocardium) is made more resistant to the damaging effects of a prolonged period of reduced blood flow (ischemia) or oxygen deprivation (hypoxia), followed by reperfusion (restoration of blood flow). This resistance is developed through a series of brief, controlled episodes of ischemia and reperfusion, which act as "preconditioning" stimuli, protecting the myocardium from subsequent more severe ischemic events. The adaptive responses triggered during preconditioning include the activation of various protective signaling pathways, release of protective factors, and modulation of cellular metabolism, ultimately leading to reduced infarct size, improved contractile function, and attenuated reperfusion injury in the myocardium.

In medical terms, suction refers to the process of creating and maintaining a partial vacuum in order to remove fluids or gases from a body cavity or wound. This is typically accomplished using specialized medical equipment such as a suction machine, which uses a pump to create the vacuum, and a variety of different suction tips or catheters that can be inserted into the area being treated.

Suction is used in a wide range of medical procedures and treatments, including wound care, surgical procedures, respiratory therapy, and diagnostic tests. It can help to remove excess fluids such as blood or pus from a wound, clear secretions from the airways during mechanical ventilation, or provide a means of visualizing internal structures during endoscopic procedures.

It is important to use proper technique when performing suctioning, as excessive or improperly applied suction can cause tissue damage or bleeding. Medical professionals are trained in the safe and effective use of suction equipment and techniques to minimize risks and ensure optimal patient outcomes.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Coronary balloon angioplasty is a minimally invasive medical procedure used to widen narrowed or obstructed coronary arteries (the blood vessels that supply oxygen-rich blood to the heart muscle) and improve blood flow to the heart. This procedure is typically performed in conjunction with the insertion of a stent, a small mesh tube that helps keep the artery open.

During coronary balloon angioplasty, a thin, flexible catheter with a deflated balloon at its tip is inserted into a blood vessel, usually through a small incision in the groin or arm. The catheter is then guided to the narrowed or obstructed section of the coronary artery. Once in position, the balloon is inflated to compress the plaque against the artery wall and widen the lumen (the inner space) of the artery. This helps restore blood flow to the heart muscle.

The procedure is typically performed under local anesthesia and conscious sedation to minimize discomfort. Coronary balloon angioplasty is a relatively safe and effective treatment for many people with coronary artery disease, although complications such as bleeding, infection, or re-narrowing of the artery (restenosis) can occur in some cases.

Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.

During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.

ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.

A brain injury is defined as damage to the brain that occurs following an external force or trauma, such as a blow to the head, a fall, or a motor vehicle accident. Brain injuries can also result from internal conditions, such as lack of oxygen or a stroke. There are two main types of brain injuries: traumatic and acquired.

Traumatic brain injury (TBI) is caused by an external force that results in the brain moving within the skull or the skull being fractured. Mild TBIs may result in temporary symptoms such as headaches, confusion, and memory loss, while severe TBIs can cause long-term complications, including physical, cognitive, and emotional impairments.

Acquired brain injury (ABI) is any injury to the brain that occurs after birth and is not hereditary, congenital, or degenerative. ABIs are often caused by medical conditions such as strokes, tumors, anoxia (lack of oxygen), or infections.

Both TBIs and ABIs can range from mild to severe and may result in a variety of physical, cognitive, and emotional symptoms that can impact a person's ability to perform daily activities and function independently. Treatment for brain injuries typically involves a multidisciplinary approach, including medical management, rehabilitation, and supportive care.

Ischemic preconditioning is a phenomenon in which brief, non-lethal episodes of ischemia (restriction or interruption of blood supply to an organ or tissue) render the tissue more resistant to subsequent prolonged ischemia and reperfusion injury. This adaptive response involves a complex series of cellular and molecular changes that protect the myocardium, brain, kidney, or other organs from ischemic damage. The underlying mechanisms include the activation of various signaling pathways, such as adenosine, opioid, and kinase pathways, which lead to the production of protective factors and the modulation of cellular responses to ischemia and reperfusion injury. Ischemic preconditioning has been extensively studied in the context of cardiovascular medicine, where it has been shown to reduce infarct size and improve cardiac function after myocardial infarction. However, this protective phenomenon has also been observed in other organs and systems, including the brain, kidney, liver, and skeletal muscle.

Left ventricular function refers to the ability of the left ventricle (the heart's lower-left chamber) to contract and relax, thereby filling with and ejecting blood. The left ventricle is responsible for pumping oxygenated blood to the rest of the body. Its function is evaluated by measuring several parameters, including:

1. Ejection fraction (EF): This is the percentage of blood that is pumped out of the left ventricle with each heartbeat. A normal ejection fraction ranges from 55% to 70%.
2. Stroke volume (SV): The amount of blood pumped by the left ventricle in one contraction. A typical SV is about 70 mL/beat.
3. Cardiac output (CO): The total volume of blood that the left ventricle pumps per minute, calculated as the product of stroke volume and heart rate. Normal CO ranges from 4 to 8 L/minute.

Assessment of left ventricular function is crucial in diagnosing and monitoring various cardiovascular conditions such as heart failure, coronary artery disease, valvular heart diseases, and cardiomyopathies.

Perfusion, in medical terms, refers to the process of circulating blood through the body's organs and tissues to deliver oxygen and nutrients and remove waste products. It is a measure of the delivery of adequate blood flow to specific areas or tissues in the body. Perfusion can be assessed using various methods, including imaging techniques like computed tomography (CT) scans, magnetic resonance imaging (MRI), and perfusion scintigraphy.

Perfusion is critical for maintaining proper organ function and overall health. When perfusion is impaired or inadequate, it can lead to tissue hypoxia, acidosis, and cell death, which can result in organ dysfunction or failure. Conditions that can affect perfusion include cardiovascular disease, shock, trauma, and certain surgical procedures.

Induced heart arrest, also known as controlled cardiac arrest or planned cardiac arrest, is a deliberate medical intervention where cardiac activity is temporarily stopped through the use of medications or electrical disruption. This procedure is typically carried out during a surgical procedure, such as open-heart surgery, where the heart needs to be stilled to allow surgeons to work on it safely.

The most common method used to induce heart arrest is by administering a medication called potassium chloride, which stops the heart's electrical activity. Alternatively, an electrical shock may be delivered to the heart to achieve the same effect. Once the procedure is complete, the heart can be restarted using various resuscitation techniques, such as defibrillation or medication administration.

It's important to note that induced heart arrest is a carefully monitored and controlled medical procedure carried out by trained healthcare professionals in a hospital setting. It should not be confused with sudden cardiac arrest, which is an unexpected and often unpredictable event that occurs outside of a medical setting.

Thrombolytic therapy, also known as thrombolysis, is a medical treatment that uses medications called thrombolytics or fibrinolytics to dissolve or break down blood clots (thrombi) in blood vessels. These clots can obstruct the flow of blood to vital organs such as the heart, lungs, or brain, leading to serious conditions like myocardial infarction (heart attack), pulmonary embolism, or ischemic stroke.

The goal of thrombolytic therapy is to restore blood flow as quickly and efficiently as possible to prevent further damage to the affected organ and potentially save lives. Commonly used thrombolytic drugs include alteplase (tPA), reteplase, and tenecteplase. It's essential to administer these medications as soon as possible after the onset of symptoms for optimal treatment outcomes. However, there are risks associated with thrombolytic therapy, such as an increased chance of bleeding complications, which must be carefully weighed against its benefits in each individual case.

Coronary vessels refer to the network of blood vessels that supply oxygenated blood and nutrients to the heart muscle, also known as the myocardium. The two main coronary arteries are the left main coronary artery and the right coronary artery.

The left main coronary artery branches off into the left anterior descending artery (LAD) and the left circumflex artery (LCx). The LAD supplies blood to the front of the heart, while the LCx supplies blood to the side and back of the heart.

The right coronary artery supplies blood to the right lower part of the heart, including the right atrium and ventricle, as well as the back of the heart.

Coronary vessel disease (CVD) occurs when these vessels become narrowed or blocked due to the buildup of plaque, leading to reduced blood flow to the heart muscle. This can result in chest pain, shortness of breath, or a heart attack.

Coronary angiography is a medical procedure that uses X-ray imaging to visualize the coronary arteries, which supply blood to the heart muscle. During the procedure, a thin, flexible catheter is inserted into an artery in the arm or groin and threaded through the blood vessels to the heart. A contrast dye is then injected through the catheter, and X-ray images are taken as the dye flows through the coronary arteries. These images can help doctors diagnose and treat various heart conditions, such as blockages or narrowing of the arteries, that can lead to chest pain or heart attacks. It is also known as coronary arteriography or cardiac catheterization.

Necrosis is the premature death of cells or tissues due to damage or injury, such as from infection, trauma, infarction (lack of blood supply), or toxic substances. It's a pathological process that results in the uncontrolled and passive degradation of cellular components, ultimately leading to the release of intracellular contents into the extracellular space. This can cause local inflammation and may lead to further tissue damage if not treated promptly.

There are different types of necrosis, including coagulative, liquefactive, caseous, fat, fibrinoid, and gangrenous necrosis, each with distinct histological features depending on the underlying cause and the affected tissues or organs.

Ischemia is the medical term used to describe a lack of blood flow to a part of the body, often due to blocked or narrowed blood vessels. This can lead to a shortage of oxygen and nutrients in the tissues, which can cause them to become damaged or die. Ischemia can affect many different parts of the body, including the heart, brain, legs, and intestines. Symptoms of ischemia depend on the location and severity of the blockage, but they may include pain, cramping, numbness, weakness, or coldness in the affected area. In severe cases, ischemia can lead to tissue death (gangrene) or organ failure. Treatment for ischemia typically involves addressing the underlying cause of the blocked blood flow, such as through medication, surgery, or lifestyle changes.

Creatine kinase (CK) is an enzyme found in various cells throughout the body, including heart muscle cells and skeletal muscle fibers. The CK enzyme exists in different forms, depending on the type of tissue where it is found. One such form is creatine kinase MB (CK-MB), which is primarily found in cardiac muscle cells.

An increase in the levels of CK-MB in the blood can indicate damage to the heart muscle, such as that caused by a heart attack or myocardial infarction. When heart muscle cells are damaged, they release their contents, including CK-MB, into the bloodstream. Therefore, measuring CK-MB levels is a useful diagnostic tool for detecting and monitoring heart muscle damage.

It's important to note that while an elevated CK-MB level can suggest heart muscle damage, it is not specific to the heart and can also be elevated in other conditions such as skeletal muscle damage or certain muscle disorders. Therefore, CK-MB levels should be interpreted in conjunction with other clinical findings and diagnostic tests.

I'm happy to help! However, it seems like there are two terms combined into one request: "Mitochondria" and "Heart." I will provide separate definitions for each.

Mitochondrion (singular) or Mitochondria (plural): These are specialized structures found in the cytoplasm of most eukaryotic cells (cells with a true nucleus), including human cells. They are often referred to as the "powerhouse" of the cell because they generate energy in the form of ATP (adenosine triphosphate) through a process called oxidative phosphorylation. Mitochondria contain their own DNA, which is distinct from the nuclear DNA, and are believed to have originated from ancient bacteria that established a symbiotic relationship with primitive eukaryotic cells.

Heart: In human anatomy, the heart is a muscular organ responsible for pumping blood throughout the body. It is located in the thoracic cavity, slightly left of the center, and is enclosed by the pericardium, a double-walled sac that provides protection and lubrication for the heart's movement. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it to the rest of the body. The heart's pumping action is regulated by electrical signals that originate in a group of specialized cardiac muscle cells called the sinoatrial node (SA node).

Cardiac myocytes are the muscle cells that make up the heart muscle, also known as the myocardium. These specialized cells are responsible for contracting and relaxing in a coordinated manner to pump blood throughout the body. They differ from skeletal muscle cells in several ways, including their ability to generate their own electrical impulses, which allows the heart to function as an independent rhythmical pump. Cardiac myocytes contain sarcomeres, the contractile units of the muscle, and are connected to each other by intercalated discs that help coordinate contraction and ensure the synchronous beating of the heart.

An anterior wall myocardial infarction (AMI) is a type of heart attack that occurs when there is a significant reduction or complete blockage of blood flow to the front wall of the heart muscle, also known as the anterior wall of the left ventricle. This reduction or blockage in blood flow is typically caused by a buildup of fatty deposits, called plaques, in the coronary arteries that supply oxygen-rich blood to the heart muscle.

When a plaque ruptures or breaks open, a blood clot forms around it, which can completely block the flow of blood to the heart muscle. This lack of blood flow causes the heart muscle to start to die, leading to a myocardial infarction or heart attack.

An anterior wall myocardial infarction is often associated with more severe symptoms and a higher risk of complications than other types of heart attacks because it affects a larger area of the heart muscle. Symptoms may include chest pain, shortness of breath, nausea, vomiting, sweating, and anxiety.

Immediate medical attention is necessary for an anterior wall myocardial infarction to restore blood flow to the heart muscle as quickly as possible and prevent further damage. Treatment options may include medications, such as clot-busting drugs or blood thinners, as well as procedures such as angioplasty or coronary artery bypass surgery.

Coronary thrombosis is a medical condition that refers to the formation of a blood clot (thrombus) inside a coronary artery, which supplies oxygenated blood to the heart muscle. The development of a thrombus can partially or completely obstruct blood flow, leading to insufficient oxygen supply to the heart muscle. This can cause chest pain (angina) or a heart attack (myocardial infarction), depending on the severity and duration of the blockage.

Coronary thrombosis often results from the rupture of an atherosclerotic plaque, a buildup of cholesterol, fat, calcium, and other substances in the inner lining (endothelium) of the coronary artery. The ruptured plaque exposes the underlying tissue to the bloodstream, triggering the coagulation cascade and resulting in the formation of a thrombus.

Immediate medical attention is crucial for managing coronary thrombosis, as timely treatment can help restore blood flow, prevent further damage to the heart muscle, and reduce the risk of complications such as heart failure or life-threatening arrhythmias. Treatment options may include medications, such as antiplatelet agents, anticoagulants, and thrombolytic drugs, or interventional procedures like angioplasty and stenting to open the blocked artery. In some cases, surgical intervention, such as coronary artery bypass grafting (CABG), may be necessary.

Mitochondrial membrane transport proteins are a type of integral membrane proteins located in the inner and outer mitochondrial membranes. They play a crucial role in the regulation of molecule exchange between the cytosol and the mitochondrial matrix, allowing only specific ions and molecules to pass through while maintaining the structural and functional integrity of the mitochondria.

The inner mitochondrial membrane transport proteins, also known as the mitochondrial carrier proteins or the solute carriers, are a family of about 50 different types of proteins that facilitate the passage of various metabolites, such as nucleotides, amino acids, fatty acids, and inorganic ions (like calcium, sodium, and potassium). These transport proteins usually function as exchangers or uniporters, moving one type of solute in one direction in exchange for another type of solute or a proton.

The outer mitochondrial membrane is more permeable than the inner membrane due to the presence of voltage-dependent anion channels (VDACs) and other porins that allow small molecules, ions, and metabolites to pass through. VDACs are the most abundant proteins in the outer mitochondrial membrane and play a significant role in controlling the flow of metabolites between the cytosol and the intermembrane space.

In summary, mitochondrial membrane transport proteins are essential for maintaining the proper functioning of mitochondria by regulating the movement of molecules across the inner and outer membranes. They facilitate the exchange of nutrients, metabolites, and ions required for oxidative phosphorylation, energy production, and other cellular processes.

Percutaneous Coronary Intervention (PCI), also known as coronary angioplasty, is a non-surgical procedure that opens up clogged coronary arteries to improve blood flow to the heart. It involves inserting a thin, flexible catheter into an artery in the groin or wrist and guiding it to the blocked artery in the heart. A small balloon is then inflated to widen the narrowed or blocked artery, and sometimes a stent (a tiny mesh tube) is placed to keep the artery open. This procedure helps to restore and maintain blood flow to the heart muscle, reducing symptoms of angina and improving overall cardiac function.

Athletic injuries are damages or injuries to the body that occur while participating in sports, physical activities, or exercise. These injuries can be caused by a variety of factors, including:

1. Trauma: Direct blows, falls, collisions, or crushing injuries can cause fractures, dislocations, contusions, lacerations, or concussions.
2. Overuse: Repetitive motions or stress on a particular body part can lead to injuries such as tendonitis, stress fractures, or muscle strains.
3. Poor technique: Using incorrect form or technique during exercise or sports can put additional stress on muscles, joints, and ligaments, leading to injury.
4. Inadequate warm-up or cool-down: Failing to properly prepare the body for physical activity or neglecting to cool down afterwards can increase the risk of injury.
5. Lack of fitness or flexibility: Insufficient strength, endurance, or flexibility can make individuals more susceptible to injuries during sports and exercise.
6. Environmental factors: Extreme weather conditions, poor field or court surfaces, or inadequate equipment can contribute to the risk of athletic injuries.

Common athletic injuries include ankle sprains, knee injuries, shoulder dislocations, tennis elbow, shin splints, and concussions. Proper training, warm-up and cool-down routines, use of appropriate protective gear, and attention to technique can help prevent many athletic injuries.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Microcirculation is the circulation of blood in the smallest blood vessels, including arterioles, venules, and capillaries. It's responsible for the delivery of oxygen and nutrients to the tissues and the removal of waste products. The microcirculation plays a crucial role in maintaining tissue homeostasis and is regulated by various physiological mechanisms such as autonomic nervous system activity, local metabolic factors, and hormones.

Impairment of microcirculation can lead to tissue hypoxia, inflammation, and organ dysfunction, which are common features in several diseases, including diabetes, hypertension, sepsis, and ischemia-reperfusion injury. Therefore, understanding the structure and function of the microcirculation is essential for developing new therapeutic strategies to treat these conditions.

Spinal cord injuries (SCI) refer to damage to the spinal cord that results in a loss of function, such as mobility or feeling. This injury can be caused by direct trauma to the spine or by indirect damage resulting from disease or degeneration of surrounding bones, tissues, or blood vessels. The location and severity of the injury on the spinal cord will determine which parts of the body are affected and to what extent.

The effects of SCI can range from mild sensory changes to severe paralysis, including loss of motor function, autonomic dysfunction, and possible changes in sensation, strength, and reflexes below the level of injury. These injuries are typically classified as complete or incomplete, depending on whether there is any remaining function below the level of injury.

Immediate medical attention is crucial for spinal cord injuries to prevent further damage and improve the chances of recovery. Treatment usually involves immobilization of the spine, medications to reduce swelling and pressure, surgery to stabilize the spine, and rehabilitation to help regain lost function. Despite advances in treatment, SCI can have a significant impact on a person's quality of life and ability to perform daily activities.

Malondialdehyde (MDA) is a naturally occurring organic compound that is formed as a byproduct of lipid peroxidation, a process in which free radicals or reactive oxygen species react with polyunsaturated fatty acids. MDA is a highly reactive aldehyde that can modify proteins, DNA, and other biomolecules, leading to cellular damage and dysfunction. It is often used as a marker of oxidative stress in biological systems and has been implicated in the development of various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders.

Acute kidney injury (AKI), also known as acute renal failure, is a rapid loss of kidney function that occurs over a few hours or days. It is defined as an increase in the serum creatinine level by 0.3 mg/dL within 48 hours or an increase in the creatinine level to more than 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days, or a urine volume of less than 0.5 mL/kg per hour for six hours.

AKI can be caused by a variety of conditions, including decreased blood flow to the kidneys, obstruction of the urinary tract, exposure to toxic substances, and certain medications. Symptoms of AKI may include decreased urine output, fluid retention, electrolyte imbalances, and metabolic acidosis. Treatment typically involves addressing the underlying cause of the injury and providing supportive care, such as dialysis, to help maintain kidney function until the injury resolves.

Warm ischemia, also known as warm injury or warm hypoxia, refers to the damage that occurs to tissues when there is an inadequate blood supply at body temperature. This can happen during surgical procedures, trauma, or other medical conditions that restrict blood flow to a specific area of the body. The lack of oxygen and nutrients, combined with the buildup of waste products, can cause cells to become damaged or die, leading to tissue dysfunction or failure.

The term "warm" is used to distinguish this type of ischemia from cold ischemia, which occurs when tissues are cooled and blood flow is restricted. Cold ischemia is often used in organ transplantation to preserve the organ until it can be transplanted. Warm ischemia is generally more damaging to tissues than cold ischemia because the metabolic demands of the cells are not being met, leading to a more rapid onset of cellular damage.

The severity and duration of warm ischemia can affect the extent of tissue damage and the likelihood of recovery. In some cases, warm ischemia may be reversible if blood flow is restored quickly enough, but in other cases it may lead to permanent tissue damage or loss of function. Treatment for warm ischemia typically involves restoring blood flow to the affected area as soon as possible, along with supportive care to manage any complications that may arise.

Lung injury, also known as pulmonary injury, refers to damage or harm caused to the lung tissue, blood vessels, or air sacs (alveoli) in the lungs. This can result from various causes such as infection, trauma, exposure to harmful substances, or systemic diseases. Common types of lung injuries include acute respiratory distress syndrome (ARDS), pneumonia, and chemical pneumonitis. Symptoms may include difficulty breathing, cough, chest pain, and decreased oxygen levels in the blood. Treatment depends on the underlying cause and may include medications, oxygen therapy, or mechanical ventilation.

In the context of medicine and toxicology, protective agents are substances that provide protection against harmful or damaging effects of other substances. They can work in several ways, such as:

1. Binding to toxic substances: Protective agents can bind to toxic substances, rendering them inactive or less active, and preventing them from causing harm. For example, activated charcoal is sometimes used in the emergency treatment of certain types of poisoning because it can bind to certain toxins in the stomach and intestines and prevent their absorption into the body.
2. Increasing elimination: Protective agents can increase the elimination of toxic substances from the body, for example by promoting urinary or biliary excretion.
3. Reducing oxidative stress: Antioxidants are a type of protective agent that can reduce oxidative stress caused by free radicals and reactive oxygen species (ROS). These agents can protect cells and tissues from damage caused by oxidation.
4. Supporting organ function: Protective agents can support the function of organs that have been damaged by toxic substances, for example by improving blood flow or reducing inflammation.

Examples of protective agents include chelating agents, antidotes, free radical scavengers, and anti-inflammatory drugs.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

I believe there may be some confusion in your question. "Rabbits" is a common name used to refer to the Lagomorpha species, particularly members of the family Leporidae. They are small mammals known for their long ears, strong legs, and quick reproduction.

However, if you're referring to "rabbits" in a medical context, there is a term called "rabbit syndrome," which is a rare movement disorder characterized by repetitive, involuntary movements of the fingers, resembling those of a rabbit chewing. It is also known as "finger-chewing chorea." This condition is usually associated with certain medications, particularly antipsychotics, and typically resolves when the medication is stopped or adjusted.

Immunoglobulin (Ig) Fab fragments are the antigen-binding portions of an antibody that result from the digestion of the whole antibody molecule by enzymes such as papain. An antibody, also known as an immunoglobulin, is a Y-shaped protein produced by the immune system to identify and neutralize foreign substances like bacteria, viruses, or toxins. The antibody has two identical antigen-binding sites, located at the tips of the two shorter arms, which can bind specifically to a target antigen.

Fab fragments are formed when an antibody is cleaved by papain, resulting in two Fab fragments and one Fc fragment. Each Fab fragment contains one antigen-binding site, composed of a variable region (Fv) and a constant region (C). The Fv region is responsible for the specificity and affinity of the antigen binding, while the C region contributes to the effector functions of the antibody.

Fab fragments are often used in various medical applications, such as immunodiagnostics and targeted therapies, due to their ability to bind specifically to target antigens without triggering an immune response or other effector functions associated with the Fc region.

The platelet glycoprotein GPIIb-IIIa complex, also known as integrin αIIbβ3 or CD41/CD61, is a heterodimeric transmembrane receptor found on the surface of platelets and megakaryocytes. It plays a crucial role in platelet aggregation and thrombus formation during hemostasis and pathological conditions such as arterial thrombosis.

The GPIIb-IIIa complex is composed of two non-covalently associated subunits, GPIIb (αIIb or CD41) and IIIa (β3 or CD61). Upon platelet activation by various agonists like ADP, thrombin, or collagen, the GPIIb-IIIa complex undergoes a conformational change that allows it to bind fibrinogen, von Willebrand factor, and other adhesive proteins. This binding event leads to platelet aggregation and the formation of a hemostatic plug or pathological thrombus.

Inhibition of the GPIIb-IIIa complex has been a target for antiplatelet therapy in the prevention and treatment of arterial thrombosis, such as myocardial infarction and stroke. Several pharmacological agents, including monoclonal antibodies and small molecule antagonists, have been developed to block this complex and reduce platelet aggregation.

"Swine" is a common term used to refer to even-toed ungulates of the family Suidae, including domestic pigs and wild boars. However, in a medical context, "swine" often appears in the phrase "swine flu," which is a strain of influenza virus that typically infects pigs but can also cause illness in humans. The 2009 H1N1 pandemic was caused by a new strain of swine-origin influenza A virus, which was commonly referred to as "swine flu." It's important to note that this virus is not transmitted through eating cooked pork products; it spreads from person to person, mainly through respiratory droplets produced when an infected person coughs or sneezes.

Echocardiography is a medical procedure that uses sound waves to produce detailed images of the heart's structure, function, and motion. It is a non-invasive test that can help diagnose various heart conditions, such as valve problems, heart muscle damage, blood clots, and congenital heart defects.

During an echocardiogram, a transducer (a device that sends and receives sound waves) is placed on the chest or passed through the esophagus to obtain images of the heart. The sound waves produced by the transducer bounce off the heart structures and return to the transducer, which then converts them into electrical signals that are processed to create images of the heart.

There are several types of echocardiograms, including:

* Transthoracic echocardiography (TTE): This is the most common type of echocardiogram and involves placing the transducer on the chest.
* Transesophageal echocardiography (TEE): This type of echocardiogram involves passing a specialized transducer through the esophagus to obtain images of the heart from a closer proximity.
* Stress echocardiography: This type of echocardiogram is performed during exercise or medication-induced stress to assess how the heart functions under stress.
* Doppler echocardiography: This type of echocardiogram uses sound waves to measure blood flow and velocity in the heart and blood vessels.

Echocardiography is a valuable tool for diagnosing and managing various heart conditions, as it provides detailed information about the structure and function of the heart. It is generally safe, non-invasive, and painless, making it a popular choice for doctors and patients alike.

Brain ischemia is the medical term used to describe a reduction or interruption of blood flow to the brain, leading to a lack of oxygen and glucose delivery to brain tissue. This can result in brain damage or death of brain cells, known as infarction. Brain ischemia can be caused by various conditions such as thrombosis (blood clot formation), embolism (obstruction of a blood vessel by a foreign material), or hypoperfusion (reduced blood flow). The severity and duration of the ischemia determine the extent of brain damage. Symptoms can range from mild, such as transient ischemic attacks (TIAs or "mini-strokes"), to severe, including paralysis, speech difficulties, loss of consciousness, and even death. Immediate medical attention is required for proper diagnosis and treatment to prevent further damage and potential long-term complications.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.

The Injury Severity Score (ISS) is a medical scoring system used to assess the severity of trauma in patients with multiple injuries. It's based on the Abbreviated Injury Scale (AIS), which classifies each injury by body region on a scale from 1 (minor) to 6 (maximum severity).

The ISS is calculated by summing the squares of the highest AIS score in each of the three most severely injured body regions. The possible ISS ranges from 0 to 75, with higher scores indicating more severe injuries. An ISS over 15 is generally considered a significant injury, and an ISS over 25 is associated with a high risk of mortality. It's important to note that the ISS has limitations, as it doesn't consider the number or type of injuries within each body region, only the most severe one.

Neutrophil infiltration is a pathological process characterized by the accumulation of neutrophils, a type of white blood cell, in tissue. It is a common feature of inflammation and occurs in response to infection, injury, or other stimuli that trigger an immune response. Neutrophils are attracted to the site of tissue damage by chemical signals called chemokines, which are released by damaged cells and activated immune cells. Once they reach the site of inflammation, neutrophils help to clear away damaged tissue and microorganisms through a process called phagocytosis. However, excessive or prolonged neutrophil infiltration can also contribute to tissue damage and may be associated with various disease states, including cancer, autoimmune disorders, and ischemia-reperfusion injury.

Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.

L-Lactate Dehydrogenase (LDH) is an enzyme found in various tissues within the body, including the heart, liver, kidneys, muscles, and brain. It plays a crucial role in the process of energy production, particularly during anaerobic conditions when oxygen levels are low.

In the presence of the coenzyme NADH, LDH catalyzes the conversion of pyruvate to lactate, generating NAD+ as a byproduct. Conversely, in the presence of NAD+, LDH can convert lactate back to pyruvate using NADH. This reversible reaction is essential for maintaining the balance between lactate and pyruvate levels within cells.

Elevated blood levels of LDH may indicate tissue damage or injury, as this enzyme can be released into the circulation following cellular breakdown. As a result, LDH is often used as a nonspecific biomarker for various medical conditions, such as myocardial infarction (heart attack), liver disease, muscle damage, and certain types of cancer. However, it's important to note that an isolated increase in LDH does not necessarily pinpoint the exact location or cause of tissue damage, and further diagnostic tests are usually required for confirmation.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Leg injuries refer to damages or harm caused to any part of the lower extremity, including the bones, muscles, tendons, ligaments, blood vessels, and other soft tissues. These injuries can result from various causes such as trauma, overuse, or degenerative conditions. Common leg injuries include fractures, dislocations, sprains, strains, contusions, and cuts. Symptoms may include pain, swelling, bruising, stiffness, weakness, or difficulty walking. The specific treatment for a leg injury depends on the type and severity of the injury.

Cold ischemia is a medical term that refers to the loss of blood flow and subsequent lack of oxygen delivery to an organ or tissue, which is then cooled and stored in a solution at temperatures between 0-4°C (32-39°F) for the purpose of transplantation. The term "cold" indicates the temperature range, while "ischemia" refers to the lack of blood flow and oxygen delivery to the tissue.

During cold ischemia, the metabolic activity of the organ or tissue slows down significantly, which helps to reduce the rate of cellular damage that would otherwise occur due to the absence of oxygen and nutrients. However, even with cold storage, there is still some degree of injury to the organ or tissue, and this can affect its function after transplantation.

The duration of cold ischemia time is an important factor in determining the success of a transplant procedure. Prolonged cold ischemia times are associated with increased risk of poor organ function and rejection, as well as decreased graft survival rates. Therefore, it is essential to minimize the cold ischemia time as much as possible during organ transplantation to ensure optimal outcomes for the recipient.

Organ preservation is a medical technique used to maintain the viability and functionality of an organ outside the body for a certain period, typically for transplantation purposes. This process involves cooling the organ to slow down its metabolic activity and prevent tissue damage, while using specialized solutions that help preserve the organ's structure and function. Commonly preserved organs include hearts, livers, kidneys, lungs, and pancreases. The goal of organ preservation is to ensure that the transplanted organ remains in optimal condition until it can be successfully implanted into a recipient.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Cytoprotection refers to the protection of cells, particularly from harmful agents or damaging conditions. This can be achieved through various mechanisms, such as:

1. Activation of cellular defense pathways that help cells resist damage.
2. Inhibition of oxidative stress and inflammation, which can cause cellular damage.
3. Enhancement of cell repair processes, enabling cells to recover from damage more effectively.
4. Prevention of apoptosis (programmed cell death) or promotion of cell survival signals.

In the medical context, cytoprotective agents are often used to protect tissues and organs from injury due to various factors like chemotherapy, radiation therapy, ischemia-reperfusion injury, or inflammation. These agents can include antioxidants, anti-inflammatory drugs, growth factors, and other compounds that help maintain cellular integrity and function.

Organ preservation solutions are specialized fluids used to maintain the viability and functionality of organs ex vivo (outside the body) during the process of transplantation. These solutions are designed to provide optimal conditions for the organ by preventing tissue damage, reducing metabolic activity, and minimizing ischemic injuries that may occur during the time between organ removal from the donor and implantation into the recipient.

The composition of organ preservation solutions typically includes various ingredients such as:

1. Cryoprotectants: These help prevent ice crystal formation and damage to cell membranes during freezing and thawing processes, especially for organs like the heart and lungs that require deep hypothermia for preservation.
2. Buffers: They maintain physiological pH levels and counteract acidosis caused by anaerobic metabolism in the absence of oxygen supply.
3. Colloids: These substances, such as hydroxyethyl starch or dextran, help preserve oncotic pressure and prevent cellular edema.
4. Electrolytes: Balanced concentrations of ions like sodium, potassium, calcium, magnesium, chloride, and bicarbonate are essential for maintaining physiological osmolarity and membrane potentials.
5. Energy substrates: Glucose, lactate, or other energy-rich compounds can serve as fuel sources to support the metabolic needs of the organ during preservation.
6. Antioxidants: These agents protect against oxidative stress and lipid peroxidation induced by ischemia-reperfusion injuries.
7. Anti-inflammatory agents and immunosuppressants: Some solutions may contain substances that mitigate the inflammatory response and reduce immune activation in the transplanted organ.

Examples of commonly used organ preservation solutions include University of Wisconsin (UW) solution, Histidine-Tryptophan-Ketoglutarate (HTK) solution, Custodiol HTK solution, and Euro-Collins solution. The choice of preservation solution depends on the specific organ being transplanted and the duration of preservation required.

Acute Lung Injury (ALI) is a medical condition characterized by inflammation and damage to the lung tissue, which can lead to difficulty breathing and respiratory failure. It is often caused by direct or indirect injury to the lungs, such as pneumonia, sepsis, trauma, or inhalation of harmful substances.

The symptoms of ALI include shortness of breath, rapid breathing, cough, and low oxygen levels in the blood. The condition can progress rapidly and may require mechanical ventilation to support breathing. Treatment typically involves addressing the underlying cause of the injury, providing supportive care, and managing symptoms.

In severe cases, ALI can lead to Acute Respiratory Distress Syndrome (ARDS), a more serious and life-threatening condition that requires intensive care unit (ICU) treatment.

Medical Definition:

Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of superoxide radicals (O2-) into oxygen (O2) and hydrogen peroxide (H2O2). This essential antioxidant defense mechanism helps protect the body's cells from damage caused by reactive oxygen species (ROS), which are produced during normal metabolic processes and can lead to oxidative stress when their levels become too high.

There are three main types of superoxide dismutase found in different cellular locations:
1. Copper-zinc superoxide dismutase (CuZnSOD or SOD1) - Present mainly in the cytoplasm of cells.
2. Manganese superoxide dismutase (MnSOD or SOD2) - Located within the mitochondrial matrix.
3. Extracellular superoxide dismutase (EcSOD or SOD3) - Found in the extracellular spaces, such as blood vessels and connective tissues.

Imbalances in SOD levels or activity have been linked to various pathological conditions, including neurodegenerative diseases, cancer, and aging-related disorders.

Alanine transaminase (ALT) is a type of enzyme found primarily in the cells of the liver and, to a lesser extent, in the cells of other tissues such as the heart, muscles, and kidneys. Its primary function is to catalyze the reversible transfer of an amino group from alanine to another alpha-keto acid, usually pyruvate, to form pyruvate and another amino acid, usually glutamate. This process is known as the transamination reaction.

When liver cells are damaged or destroyed due to various reasons such as hepatitis, alcohol abuse, nonalcoholic fatty liver disease, or drug-induced liver injury, ALT is released into the bloodstream. Therefore, measuring the level of ALT in the blood is a useful diagnostic tool for evaluating liver function and detecting liver damage. Normal ALT levels vary depending on the laboratory, but typically range from 7 to 56 units per liter (U/L) for men and 6 to 45 U/L for women. Elevated ALT levels may indicate liver injury or disease, although other factors such as muscle damage or heart disease can also cause elevations in ALT.

Aspartate aminotransferases (ASTs) are a group of enzymes found in various tissues throughout the body, including the heart, liver, and muscles. They play a crucial role in the metabolic process of transferring amino groups between different molecules.

In medical terms, AST is often used as a blood test to measure the level of this enzyme in the serum. Elevated levels of AST can indicate damage or injury to tissues that contain this enzyme, such as the liver or heart. For example, liver disease, including hepatitis and cirrhosis, can cause elevated AST levels due to damage to liver cells. Similarly, heart attacks can also result in increased AST levels due to damage to heart muscle tissue.

It is important to note that an AST test alone cannot diagnose a specific medical condition, but it can provide valuable information when used in conjunction with other diagnostic tests and clinical evaluation.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

Prospective studies, also known as longitudinal studies, are a type of cohort study in which data is collected forward in time, following a group of individuals who share a common characteristic or exposure over a period of time. The researchers clearly define the study population and exposure of interest at the beginning of the study and follow up with the participants to determine the outcomes that develop over time. This type of study design allows for the investigation of causal relationships between exposures and outcomes, as well as the identification of risk factors and the estimation of disease incidence rates. Prospective studies are particularly useful in epidemiology and medical research when studying diseases with long latency periods or rare outcomes.

Eye injuries refer to any damage or trauma caused to the eye or its surrounding structures. These injuries can vary in severity and may include:

1. Corneal abrasions: A scratch or scrape on the clear surface of the eye (cornea).
2. Chemical burns: Occurs when chemicals come into contact with the eye, causing damage to the cornea and other structures.
3. Eyelid lacerations: Cuts or tears to the eyelid.
4. Subconjunctival hemorrhage: Bleeding under the conjunctiva, the clear membrane that covers the white part of the eye.
5. Hyphema: Accumulation of blood in the anterior chamber of the eye, which is the space between the cornea and iris.
6. Orbital fractures: Breaks in the bones surrounding the eye.
7. Retinal detachment: Separation of the retina from its underlying tissue, which can lead to vision loss if not treated promptly.
8. Traumatic uveitis: Inflammation of the uvea, the middle layer of the eye, caused by trauma.
9. Optic nerve damage: Damage to the optic nerve, which transmits visual information from the eye to the brain.

Eye injuries can result from a variety of causes, including accidents, sports-related injuries, violence, and chemical exposure. It is important to seek medical attention promptly for any suspected eye injury to prevent further damage and potential vision loss.

An animal model in medicine refers to the use of non-human animals in experiments to understand, predict, and test responses and effects of various biological and chemical interactions that may also occur in humans. These models are used when studying complex systems or processes that cannot be easily replicated or studied in human subjects, such as genetic manipulation or exposure to harmful substances. The choice of animal model depends on the specific research question being asked and the similarities between the animal's and human's biological and physiological responses. Examples of commonly used animal models include mice, rats, rabbits, guinea pigs, and non-human primates.

Coronary artery disease, often simply referred to as coronary disease, is a condition in which the blood vessels that supply oxygen-rich blood to the heart become narrowed or blocked due to the buildup of fatty deposits called plaques. This can lead to chest pain (angina), shortness of breath, or in severe cases, a heart attack.

The medical definition of coronary artery disease is:

A condition characterized by the accumulation of atheromatous plaques in the walls of the coronary arteries, leading to decreased blood flow and oxygen supply to the myocardium (heart muscle). This can result in symptoms such as angina pectoris, shortness of breath, or arrhythmias, and may ultimately lead to myocardial infarction (heart attack) or heart failure.

Risk factors for coronary artery disease include age, smoking, high blood pressure, high cholesterol, diabetes, obesity, physical inactivity, and a family history of the condition. Lifestyle changes such as quitting smoking, exercising regularly, eating a healthy diet, and managing stress can help reduce the risk of developing coronary artery disease. Medical treatments may include medications to control blood pressure, cholesterol levels, or irregular heart rhythms, as well as procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Free radicals are molecules or atoms that have one or more unpaired electrons in their outermost shell, making them highly reactive. They can be formed naturally in the body through processes such as metabolism and exercise, or they can come from external sources like pollution, radiation, and certain chemicals. Free radicals can cause damage to cells and contribute to the development of various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. Antioxidants are substances that can neutralize free radicals and help protect against their harmful effects.

Middle Cerebral Artery (MCA) infarction is a type of ischemic stroke that occurs when there is an obstruction in the blood supply to the middle cerebral artery, which is one of the major blood vessels that supplies oxygenated blood to the brain. The MCA supplies blood to a large portion of the brain, including the motor and sensory cortex, parts of the temporal and parietal lobes, and the basal ganglia.

An infarction is the death of tissue due to the lack of blood supply, which can lead to damage or loss of function in the affected areas of the brain. Symptoms of MCA infarction may include weakness or numbness on one side of the body, difficulty speaking or understanding speech, vision problems, and altered levels of consciousness.

MCA infarctions can be caused by various factors, including embolism (a blood clot that travels to the brain from another part of the body), thrombosis (a blood clot that forms in the MCA itself), or stenosis (narrowing of the artery due to atherosclerosis or other conditions). Treatment for MCA infarction may include medications to dissolve blood clots, surgery to remove the obstruction, or rehabilitation to help regain lost function.

Antioxidants are substances that can prevent or slow damage to cells caused by free radicals, which are unstable molecules that the body produces as a reaction to environmental and other pressures. Antioxidants are able to neutralize free radicals by donating an electron to them, thus stabilizing them and preventing them from causing further damage to the cells.

Antioxidants can be found in a variety of foods, including fruits, vegetables, nuts, and grains. Some common antioxidants include vitamins C and E, beta-carotene, and selenium. Antioxidants are also available as dietary supplements.

In addition to their role in protecting cells from damage, antioxidants have been studied for their potential to prevent or treat a number of health conditions, including cancer, heart disease, and age-related macular degeneration. However, more research is needed to fully understand the potential benefits and risks of using antioxidant supplements.

Neck injuries refer to damages or traumas that occur in any part of the neck, including soft tissues (muscles, ligaments, tendons), nerves, bones (vertebrae), and joints (facet joints, intervertebral discs). These injuries can result from various incidents such as road accidents, falls, sports-related activities, or work-related tasks. Common neck injuries include whiplash, strain or sprain of the neck muscles, herniated discs, fractured vertebrae, and pinched nerves, which may cause symptoms like pain, stiffness, numbness, tingling, or weakness in the neck, shoulders, arms, or hands. Immediate medical attention is necessary for proper diagnosis and treatment to prevent further complications and ensure optimal recovery.

Nitric oxide (NO) is a molecule made up of one nitrogen atom and one oxygen atom. In the body, it is a crucial signaling molecule involved in various physiological processes such as vasodilation, immune response, neurotransmission, and inhibition of platelet aggregation. It is produced naturally by the enzyme nitric oxide synthase (NOS) from the amino acid L-arginine. Inhaled nitric oxide is used medically to treat pulmonary hypertension in newborns and adults, as it helps to relax and widen blood vessels, improving oxygenation and blood flow.

Free radical scavengers, also known as antioxidants, are substances that neutralize or stabilize free radicals. Free radicals are highly reactive atoms or molecules with unpaired electrons, capable of causing damage to cells and tissues in the body through a process called oxidative stress. Antioxidants donate an electron to the free radical, thereby neutralizing it and preventing it from causing further damage. They can be found naturally in foods such as fruits, vegetables, and nuts, or they can be synthesized and used as dietary supplements. Examples of antioxidants include vitamins C and E, beta-carotene, and selenium.

Myocardial stunning is a condition in cardiovascular medicine where the heart muscle (myocardium) temporarily loses its ability to contract effectively after being exposed to a brief, severe episode of ischemia (restriction of blood supply) or reperfusion injury (damage that occurs when blood flow is restored to an organ or tissue after a period of ischemia). This results in a reduction in the heart's pumping function, which can be detected using imaging techniques such as echocardiography.

The stunning phenomenon is believed to be caused by complex biochemical and cellular processes that occur during ischemia-reperfusion injury, including the generation of free radicals, calcium overload, inflammation, and activation of various signaling pathways. These changes can lead to the dysfunction of contractile proteins, mitochondrial damage, and altered gene expression in cardiomyocytes (heart muscle cells).

Myocardial stunning is often observed following procedures such as coronary angioplasty or bypass surgery, where blood flow is temporarily interrupted and then restored to the heart. It can also occur during episodes of unstable angina, acute myocardial infarction, or cardiac arrest. Although the stunning itself is usually reversible within a few days to several weeks, it may contribute to short-term hemodynamic instability and increased risk of adverse events such as heart failure, arrhythmias, or even death.

Management of myocardial stunning typically involves supportive care, optimizing hemodynamics, and addressing any underlying conditions that may have contributed to the ischemic episode. In some cases, medications like inotropes or vasopressors might be used to support cardiac function temporarily. Preventive strategies, such as maintaining adequate blood pressure, heart rate, and oxygenation during procedures, can help reduce the risk of myocardial stunning.

Neuroprotective agents are substances that protect neurons or nerve cells from damage, degeneration, or death caused by various factors such as trauma, inflammation, oxidative stress, or excitotoxicity. These agents work through different mechanisms, including reducing the production of free radicals, inhibiting the release of glutamate (a neurotransmitter that can cause cell damage in high concentrations), promoting the growth and survival of neurons, and preventing apoptosis (programmed cell death). Neuroprotective agents have been studied for their potential to treat various neurological disorders, including stroke, traumatic brain injury, Parkinson's disease, Alzheimer's disease, and multiple sclerosis. However, more research is needed to fully understand their mechanisms of action and to develop effective therapies.

In medical terms, constriction refers to the narrowing or tightening of a body part or passageway. This can occur due to various reasons such as spasms of muscles, inflammation, or abnormal growths. It can lead to symptoms like difficulty in breathing, swallowing, or blood flow, depending on where it occurs. For example, constriction of the airways in asthma, constriction of blood vessels in hypertension, or constriction of the esophagus in certain digestive disorders.

A stent is a small mesh tube that's used to treat narrow or weak arteries. Arteries are blood vessels that carry blood away from your heart to other parts of your body. A stent is placed in an artery as part of a procedure called angioplasty. Angioplasty restores blood flow through narrowed or blocked arteries by inflating a tiny balloon inside the blocked artery to widen it.

The stent is then inserted into the widened artery to keep it open. The stent is usually made of metal, but some are coated with medication that is slowly and continuously released to help prevent the formation of scar tissue in the artery. This can reduce the chance of the artery narrowing again.

Stents are also used in other parts of the body, such as the neck (carotid artery) and kidneys (renal artery), to help maintain blood flow and prevent blockages. They can also be used in the urinary system to treat conditions like ureteropelvic junction obstruction or narrowing of the urethra.

The Predictive Value of Tests, specifically the Positive Predictive Value (PPV) and Negative Predictive Value (NPV), are measures used in diagnostic tests to determine the probability that a positive or negative test result is correct.

Positive Predictive Value (PPV) is the proportion of patients with a positive test result who actually have the disease. It is calculated as the number of true positives divided by the total number of positive results (true positives + false positives). A higher PPV indicates that a positive test result is more likely to be a true positive, and therefore the disease is more likely to be present.

Negative Predictive Value (NPV) is the proportion of patients with a negative test result who do not have the disease. It is calculated as the number of true negatives divided by the total number of negative results (true negatives + false negatives). A higher NPV indicates that a negative test result is more likely to be a true negative, and therefore the disease is less likely to be present.

The predictive value of tests depends on the prevalence of the disease in the population being tested, as well as the sensitivity and specificity of the test. A test with high sensitivity and specificity will generally have higher predictive values than a test with low sensitivity and specificity. However, even a highly sensitive and specific test can have low predictive values if the prevalence of the disease is low in the population being tested.

Yellon, D. M.; Hausenloy, D. J. (2007). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11): 1121-1135. ... After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of ... Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. The benefits of HGF therapy ... Sala, V.; Crepaldi, T. (2011). "Novel therapy for myocardial infarction: Can HGF/Met be beneficial?". Cellular and Molecular ...
Hausenloy, Derek J.; Yellon, Derek M. (31 July 2008). "Time to Take Myocardial Reperfusion Injury Seriously". New England ... Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused ... Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are ... Reperfusion injury is distinct from cerebral hyperperfusion syndrome (sometimes called "Reperfusion syndrome"), a state of ...
H 2S donors reduce myocardial injury and reperfusion complications. Increased H 2S levels within the body will react with ... Non-safety related ) "Reduction of Ischemia-Reperfusion Mediated Cardiac Injury in Subjects Undergoing Coronary Artery Bypass ... Hydrogen sulfide (H 2S) deficiency can be detrimental to the vascular function after an acute myocardial infarction (AMI). AMIs ... "IK-1001 (Sodium Sulfide (Na2S) for Injection) in Subjects With Acute ST-Segment Elevation Myocardial Infarction". ...
May 2010). "Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury". Stem Cell Research. 4 (3): 214-22. doi: ...
H 2S therapy reduces myocardial injury and reperfusion complications. Due to its effects similar to NO (without its potential ... Yang X, de Caestecker M, Otterbein LE, Wang B (July 2020). "Carbon monoxide: An emerging therapy for acute kidney injury". ... potential to be used to prevent the development of a series of pathological conditions including ischemia reperfusion injury, ... H 2S deficiency can be detrimental to the vascular function after an acute myocardial infarction (AMI). ...
"Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice". FASEB Journal. 22 (10): 3549-60. doi: ... HDIs are also being studied as protection of heart muscle in acute myocardial infarction. Miller TA, Witter DJ, Belvedere S ( ...
... a new therapeutic target for myocardial reperfusion injury". Cardiovascular Research. 111 (2): 134-141. doi:10.1093/cvr/cvw100 ... Succinate accumulation under hypoxic conditions has been implicated in the reperfusion injury through increased ROS production ... In animal models, pharmacological inhibition of ischemic succinate accumulation ameliorated ischemia-reperfusion injury. As of ... "Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS". Nature. 515 (7527): 431-5. Bibcode: ...
Alam, M.R.; D. Baetz; M. Ovize (2015). "Cyclophilin D and myocardial ischemia-reperfusion injury: a fresh perspective". J Mol ... Reperfusion injury Reperfusion therapy Eltzschig, H.K. & T. Eckle (2011). "Ischemia and reperfusion-from mechanism to ... Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, ... IR injury contributes to disease and mortality in a variety of pathologies, including myocardial infarction, ischemic stroke, ...
"Effect of trapidil in myocardial ischemia-reperfusion injury in rabbit". Indian Journal of Pharmacology. 46 (2): 207-210. doi: ...
"Nerve growth factor reduces myocardial ischemia/reperfusion injury in rat hearts". Journal of Basic and Clinical Physiology and ... and traumatic brain injury. Lazarovici also contributed to the characterization of NGF angiogenic properties and ... pan-hematopoietic subpopulation derived from human umbilical cord blood in a traumatic brain injury model". Cytotherapy. 20 (2 ...
Neuhof C, Neuhof H (2014). "Calpain system and its involvement in myocardial ischemia and reperfusion injury". World J Cardiol ... traumatic brain injury and spinal cord injury. Excessive amounts of calpain can be activated due to Ca2+ influx after ... or some types of traumatic brain injury such as diffuse axonal injury. Increase in concentration of calcium in the cell results ... Calpain may be released in the brain for up to a month after a head injury, and may be responsible for a shrinkage of the brain ...
"Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in mice". Arteriosclerosis, Thrombosis, and ...
Moens, A.L.; Claeys, M.J.; Timmermans, J.P.; Vrints, C.J. (April 2005). "Myocardial ischemia/reperfusion-injury, a clinical ... However, it is more commonly associated with reperfusion after myocardial injury. AIVR is generally considered to be a benign ... Norris, RM; Mercer, CJ (Mar-Apr 1974). "Significance of idioventricular rhythms in acute myocardial infarction". Progress in ... Accelerated idioventricular rhythm is the most common reperfusion arrhythmia in humans. However, ventricular tachycardia and ...
Yellon, Derek M.; Hausenloy, Derek J. (2007-09-13). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11 ... With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue and ... "Targeting reperfusion injury in patients with ST-segment elevation myocardial infarction: trials and tribulations". European ... "Revisiting Cerebral Postischemic Reperfusion Injury: New Insights in Understanding Reperfusion Failure, Hemorrhage, and Edema ...
A deletion of the C-terminal 19 amino acids was found during myocardial ischemia-reperfusion injury in Langendorff perfused rat ... "Troponin I degradation and covalent complex formation accompanies myocardial ischemia/reperfusion injury". Circulation Research ... It was also seen in myocardial stunning in coronary bypass patients. Over-expression of the C-terminal truncated cardiac TnI ( ... Ni CY (2002). "Cardiac troponin I: a biomarker for detection and risk stratification of minor myocardial damage". Clinical ...
"AGGF1 protects from myocardial ischemia/reperfusion injury by regulating myocardial apoptosis and angiogenesis". Apoptosis. 19 ... Additionally, AGGF1 has been shown to protect against inflammation and ischemic injuries. During embryongenesis, AGGF1 is ... for Blocking Neointimal Formation After Vascular Injury". Journal of the American Heart Association. 6 (6): e005889. doi: ... has also been implicated in treatment after vascular smooth muscle cell damage due to coronary artery disease and myocardial ...
Such injury would occur when a patient has an acute myocardial infarct followed by reperfusion by either percutaneous coronary ... ZQ, Zhao (August 2003). "Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ... in the area of coronary heart disease in an attempt to limit the injury caused to the heart via ischemia and reperfusion injury ... The second window begins at 24 hours and lasts up to 72 hours after the ischaemia and reperfusion stimulus. In an experimental ...
Myocardial damage with the resumption of blood flow after an ischemic event is termed "reperfusion injury". The mitochondrial ... Sanada S, Komuro I, Kitakaze M (November 2011). "Pathophysiology of myocardial reperfusion injury: preconditioning, ... specifically as a treatment for ischemic reperfusion injury. The rapid return of myocardial blood supply is critical in order ... reperfusion, and activation of the reperfusion injury salvage kinase pathway (RISK). The mitochondrial accumulation of ...
"Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning". ... "New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase ( ... Brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous ... These signaling events act on the ROS-generating mitochondria, activate PKCε and the Reperfusion Injury Salvage Kinase (RISK) ...
November 2013). "Role of NADPH oxidase isoforms NOX1, NOX2 and NOX4 in myocardial ischemia/reperfusion injury". Journal of ... which play a role in myocardial reperfusion injury. This was a result of the relation between Nox2 and signaling necessary for ... the protein can be a potential target for drug medication due to its negative effect on myocardial reperfusion. Recent evidence ... It has also been shown to play a part in determining the size of a myocardial infarction due to its connection to ROS, ...
"Mitochondrial connexin43 as a new player in the pathophysiology of myocardial ischaemia-reperfusion injury". Cardiovascular ... which plays a part in ventricular remolding and healing of wounds after a myocardial infarction, are present in structural ... "Reduced expression of Cx43 attenuates ventricular remodeling after myocardial infarction via impaired TGF-β signaling". ...
"Protective role of deoxyschizandrin and schisantherin a against myocardial ischemia-reperfusion injury in rats". PLOS ONE. 8 (4 ...
"Cardioprotection with forsythoside B in rat myocardial ischemia-reperfusion injury: relation to inflammation response". ... January 2019). "Protective effect of forsythoside B against lipopolysaccharide-induced acute lung injury by attenuating the ...
In addition, palmatine might have the antiarrhythmic effect, and provideprotection from myocardial ischemia-reperfusion injury ...
... protects the isolated rat heart from the myocardial injuries produced by ischemia and reperfusion. Planta Med, 1993 ... Cyclobuxine was in this way able to suppress the damage (myocardial injury) produced by ischemia. As indicated above, research ... cyclobuxine was also found to have a protective effect on myocardial cells against ischemia and reperfusion (in an isolated rat ...
A major topic of research is the impact of hydrogen sulfide on reducing myocardial ischemia-reperfusion injury. Reperfusion ... "Roles of the nitric oxide signaling pathway in cardiac ischemic preconditioning against myocardial ischemia-reperfusion injury ... Reperfusion triggers an inflammatory response and often results in oxidative damage. H2S decreases injury through many ... The mitochondria has been known to protect the heart from ischemic-reperfusion injury through the opening of the ATP-sensitive ...
Zheng, Pengfei (2017-02-20). "Plin5 alleviates myocardial ischaemia/reperfusion injury by reducing oxidative stress through ... deficiency in PLIN5 initiates excessive phosforilation of PI3K/Akt which contributes to ischemia-reperfusion injury aggravation ... Wang, Hong (2013). "Cardiomyocyte-specific perilipin 5 overexpression leads to myocardial steatosis and modest cardiac ...
... binding lectin-associated serine protease-2 confers protection from myocardial and gastrointestinal ischemia/reperfusion injury ...
"Beta3-Adrenoreceptor Stimulation Ameliorates Myocardial Ischemia-Reperfusion Injury Via Endothelial Nitric Oxide Synthase and ...
In a mouse model of infarction the A3 selective agonist CP-532,903 protected against myocardial ischemia and reperfusion injury ... protects against myocardial ischemia/reperfusion injury via the sarcolemmal ATP-sensitive potassium channel". The Journal of ... reduces ischemia/reperfusion injury in mice by activating the A3 adenosine receptor". The Journal of Pharmacology and ... it is involved in the inhibition of neutrophil degranulation in neutrophil-mediated tissue injury, it has been implicated in ...
... collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and ... While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, ... Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. ... while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing ...
... Front ... as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. Endogenous cardioprotective mechanisms against I/R ... Therefore, our aim was to develop a medium throughput comorbidity cell-based test system of myocardial I/R injury, ... Each group was then subjected to simulated ischemia/reperfusion (SI/R) or corresponding normoxic condition, respectively. ...
Researchers interested in Myocardial Reperfusion Injury
Learn about the link between a higher incidence of acute myocardial infarction and a poorer prognosis. ... Disruption of Circadian Rhythms by Shift Work Exacerbates Reperfusion Injury in Myocardial Infarction. ... A recent study discovered that shift employment causes myocardial infarction reperfusion damage. It discovered a new nuclear ... imaging after reperfusion therapy. The main outcome was the size of the CMR-defined post-reperfusion infarct. The composite of ...
... * ... Shen Y, Liu X, Shi J and Wu X: Involvement of Nrf2 in myocardial ischemia and reperfusion injury. Int J Biol Macromol. 125:496- ... Shi X, Tao G, Ji L and Tian G: Sappanone a protects against myocardial ischemia reperfusion injury by modulation of Nrf2. Drug ... Shen S, He F, Cheng C, Xu B and Sheng J: Uric acid aggravates myocardial ischemia-reperfusion injury via ROS/NLRP3 pyroptosis ...
Despite numerous studies on myocardial I/R injury, the mechanisms underlying the role of miRNAs in myocardial I/R injury remain ... 132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. The myocardial I/R model was established ... Ding M, Lei J, Han H, Li W, Qu Y, Fu E, Fu F and Wang X: SIRT1 protects against myocardial ischemia-reperfusion injury via ... despite numerous studies on myocardial I/R injury, deeper insight into the underlying mechanisms of myocardial I/R injury is ...
Oral pre-treatment with thiocyanate (SCN-) protects against myocardial ischaemia-reperfusion injury in rats. Publikation: ... Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia-reperfusion injury in rats Forlagets udgivne ... Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), ... Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global ...
Oral pre-treatment with thiocyanate (SCN-) protects against myocardial ischaemia-reperfusion injury in rats. Publikation: ... Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia-reperfusion injury in rats Forlagets udgivne ... Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), ... Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global ...
Hence, we investigated the effect of KMP in ischemia-reperfusion (IR) model of myocardial injury in rats. We studied male ... Hence, we investigated the effect of KMP in ischemia-reperfusion (IR) model of myocardial injury in rats. We studied male ... Jennings, R. B.. Historical perspective on the pathology of myocardial ischemia/reperfusion injury. Circulation Research . 2013 ... Ischemic Injury via Inhibition of MAPK Signaling Pathway in Experimental Model of Myocardial Ischemia-Reperfusion Injury" ...
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IL-36 improves age-related coronary microcirculatory dysfunction and attenuates myocardial ischemia/reperfusion injury in mice ... IL-36 improves age-related coronary microcirculatory dysfunction and attenuates myocardial ischemia/reperfusion injury in mice ... Following myocardial infarction (MI), elderly patients have a poorer prognosis than younger patients, which may be linked to ... We first demonstrated the presence of IL-36(α/β) and its receptor (IL-36R) in ischemia/reperfusion-injured (IR-injured) mouse ...
Dive into the research topics of Oxygen free radicals and myocardial reperfusion injury. Together they form a unique ...
title = "Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison",. abstract = "Myocardial ... Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison. / Hashmi, Satwat; Al-Salam, Suhail. In: ... Acute myocardial infarction and myocardial ischemia-reperfusion injury : A comparison. In: International Journal of Clinical ... Hashmi S, Al-Salam S. Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison. International ...
title = "Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison",. abstract = "Myocardial ... Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison. / Hashmi, Satwat; Al-Salam, Suhail. In: ... Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison. International Journal of Clinical and ... Acute myocardial infarction and myocardial ischemia-reperfusion injury : A comparison. In: International Journal of Clinical ...
Yellon, D. M.; Hausenloy, D. J. (2007). "Myocardial Reperfusion Injury". New England Journal of Medicine. 357 (11): 1121-1135. ... After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of ... Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. The benefits of HGF therapy ... Sala, V.; Crepaldi, T. (2011). "Novel therapy for myocardial infarction: Can HGF/Met be beneficial?". Cellular and Molecular ...
Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats. American Journal of Physiology - Heart and ... Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats. In: American Journal of Physiology - Heart ... Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats. / Zhai, Peiyong; Eurell, Thomas E.; ... Dive into the research topics of Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats. Together ...
Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ... Myocardial reperfusion injury. N Engl J Med. 2007 Sep 13. 357 (11):1121-35. [QxMD MEDLINE Link]. ... The role of reperfusion therapy in paced patients with acute myocardial infarction. Am Heart J. 2001 Sep. 142(3):516-9. [QxMD ... Should Age Be Considered with Troponin Testing for Myocardial Injury? 0.25 CME / CE / ABIM MOC Credits Clinical Review ...
Endothelial cell dysfunction after ischemic arrest and reperfusion: A possible mechanism of myocardial injury during reflow. / ... Endothelial cell dysfunction after ischemic arrest and reperfusion : A possible mechanism of myocardial injury during reflow. ... T1 - Endothelial cell dysfunction after ischemic arrest and reperfusion. T2 - A possible mechanism of myocardial injury during ... Endothelial cell dysfunction after ischemic arrest and reperfusion: A possible mechanism of myocardial injury during reflow. ...
... can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic ... and is the first to report the protection by catechin at this dose under conditions of myocardial ischemia-reperfusion injury. ... injury is an important health concern in myocardial infarction and situations such as angioplasty and cardiac surgeries. ... showed in most but not all measurements that this was a suitable model of IR injury. The treatment experiments showed that 150 ...
Atorvastatin Inhibits Fas Expression in Ischemia-Reperfusion Induced Myocardial Cell Injury ... Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat. Circulation ... shown that myocardial reperfusion itself results in enhanced myocardial injury [8, 9]. It has been demonstrated that myocardium ... Differential response to myocardial reperfusion injury in eNOS-deficient mice. Am J Physiol Heart Circ Physiol 2002; 282(6): ...
Ticagrelor protects the heart against reperfusion injury and improves remodeling after myocardial infarction. / Ye, Yumei; ... Ticagrelor protects the heart against reperfusion injury and improves remodeling after myocardial infarction. In: ... title = "Ticagrelor protects the heart against reperfusion injury and improves remodeling after myocardial infarction", ... Ticagrelor protects the heart against reperfusion injury and improves remodeling after myocardial infarction. ...
... comparative effects in myocardial ischaemic/reperfusion injury.. Together they form a unique fingerprint. ...
Myocardial Ablation of G Protein-Coupled Receptor Kinase 2 (GRK2) Decreases Ischemia/Reperfusion Injury through an Anti- ... Decreases Ischemia/Reperfusion Injury through an Anti-Intrinsic Apoptotic Pathway. Together they form a unique fingerprint. ... Dive into the research topics of Myocardial Ablation of G Protein-Coupled Receptor Kinase 2 (GRK2) ...
Following reperfusion for 6 hours, angiotensin II content of the heart was determined using radioimmunoassay. Myocardial ... telmisartan improved microvascular dysfunction during myocardial I/R injury via the PPARG pathway. ... Myocardial capillaries were examined with transmission electron microscopy. Intercellular adhesion molecule-1 (ICAM-1) and ... injury by activating the peroxisome proliferator-activated receptor gamma (PPARG) pathway. Forty-eight male rabbits were ...
... of inducible nitric oxide synthase in peripheral blood cells as a mediator of myocardial ischemia/reperfusion injury. ... of inducible nitric oxide synthase in peripheral blood cells as a mediator of myocardial ischemia/reperfusion injury. Together ...
keywords = "Akt, PKCσ, myocardial reperfusion injury, proteasome inhibition, transgenic mouse",. author = "Zongwen Tian and ... Genetically induced moderate inhibition of the proteasome in cardiomyocytes exacerbates myocardial ischemia-reperfusion injury ... Genetically induced moderate inhibition of the proteasome in cardiomyocytes exacerbates myocardial ischemia-reperfusion injury ... Genetically induced moderate inhibition of the proteasome in cardiomyocytes exacerbates myocardial ischemia-reperfusion injury ...
MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival ... 1. MicroRNA-503 (miR-503) exacerbates myocardial ischemia/reperfusion (I/R) injury by inhibiting prosurvival signaling pathways ... Other factors contributing to I/R injury Lack of sufficient evidence to support the conclusion Potential biases in the study ... 3. Agomir-503 treatment worsens hypoxia/reoxygenation-induced injuries, while antagomir-503 treatment attenuates them and ...
Interleukin-37 ameliorates myocardial ischemia/reperfusion injury in mice. Clin Exp immunol 2014; 176: 438-451. ... Beneficial effects of IL-37 after spinal cord injury in mice. Proc Natl Acad Sci USA 2016; 113: 1411-1416. ...
Exosome Secreted by MSC Reduces Myocardial Ischemia/Reperfusion Injury. Stem Cell Res. 4, 214-222 (2010). ... of MSC-Exo has greatly increased after the first report of MSC-Exo ameliorating myocardial ischemia/reperfusion injury in a ... Lai, R. C., Yeo, R. W., Tan, K. H. & Lim, S. K. Mesenchymal Stem Cell Exosome Ameliorates Reperfusion Injury through Proteomic ... Human Mesenchymal Stem Cell Microvesicles for Treatment of Escherichia Coli Endotoxin-Induced Acute Lung Injury in Mice. Stem ...
... level after acute myocardial infarction (AMI) with left ventricular dysfunction. In a double blind, randomized, placebo- ... Grech, E.D.; Jackson, M.; Ramsdale, D.R. Reperfusion injury after acute myocardial infarction. Br. Med. J. 1995, 310, 477-478 ... Bioenergetic effect of liposomal coenzyme Q10 on myocardial ischaemia reperfusion injury. Biofactors 1999, 9, 307-313. [Google ... Since coenzyme Q10 is the treatment of choice in patients with heart failure due to myocardial infarction [14,15,16,17,18], the ...
  • Involvement of Nrf2 in myocardial ischemia and reperfusion injury. (nih.gov)
  • 1.Wang W, Schulze CJ, Suarez-Pinzon WL, Dyck JR, SawickiG, Schulz R. Intracellular action of matrix metalloproteinase-2 accounts for acute myocardial ischemia and reperfusion injury. (bvsalud.org)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • Myocardial I/R injury may induce cell apoptosis and autophagy by activating oxidative stress and upregulating inflammatory mediators, ultimately resulting in irreversible fibrotic damage ( 3 ). (spandidos-publications.com)
  • In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis. (aku.edu)
  • It is produced and proteolytically cleaved to its active state in response to cellular injury or during apoptosis. (wikipedia.org)
  • Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
  • Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
  • Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • Ticagrelor, but not clopidogrel, increased myocardial adenosine levels, increased phosphorylation of Akt, endothelial NO synthase, and extracellular-signal-regulated kinase 1/2 4 hours after reperfusion and decreased apoptosis. (utmb.edu)
  • Dexmedetomidine pretreatment can obviously relieve myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis in rats probably by activating the Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway. (ijpsonline.com)
  • In rats and pigs, BSPC@HM NCs remarkably downregulates Sav1 in IR-injured myocardium, promotes myocardium regeneration, suppresses myocardial apoptosis, and recovers cardiac functions. (scimage.cn)
  • The most effective early treatment for reducing AMI injury and limiting the infarcted myocardium is timely coronary revascularization using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) [ 2 - 4 ]. (hindawi.com)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. (hindawi.com)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. (spandidos-publications.com)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of the heart, consequently reducing proper cardiac function. (wikipedia.org)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • The Canadian Cardiovascular Society (CCS) has developed a four-stage classification of acute atherothrombotic myocardial infarction (MI) based on the severity of the injury to the myocardium. (medscape.com)
  • Because the major source of CK-MB is myocardium, an elevated CK-MB level reflects myocardial injury, including acute myocardial infarction, myocarditis, cardiac trauma, cardiac surgery, and endomyocardial biopsy. (medscape.com)
  • Patients' data for the study were obtained from the EARLY-MYO-CMR (Early Assessment of Myocardial Tissue Characteristics by CMR in STEMI) registry, which was a prospective, multicenter registry of patients with ST-segment elevation myocardial infarction (STEMI) who underwent cardiac magnetic resonance (CMR) imaging after reperfusion therapy. (physiciansweekly.com)
  • Myocardial infarction (MI) denotes the death of cardiac myocytes due to extended ischemia. (aku.edu)
  • Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. (wikipedia.org)
  • Transfection with HGF plasmids in damaged cardiac tissue also promotes angiogenesis (increased capillary density compared to control subjects), as well as decreasing detrimental remodelling of the tissue at the site of injury (decreased fibrotic deposition). (wikipedia.org)
  • To determine the mechanism(s) responsible for decreased coronary flow after global cardiac ischemia and reperfusion, we studied 40 isolated rabbit hearts before and after 30 minutes of normothermic ischemic arrest and reperfusion. (elsevierpure.com)
  • Myocardial ischemia-reperfusion (I/R) injury is an important health concern in myocardial infarction and situations such as angioplasty and cardiac surgeries. (usask.ca)
  • It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
  • In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
  • The role of cardiac proteasome dysfunction during I/R and the perspective to diminish I/R injury by manipulating proteasome function remain unclear. (elsevierpure.com)
  • This study reports a bioinspired strategy to overcome the multiple systemic barriers against myocardial siRNA delivery, and holds profound potential for gene therapy against cardiac injuries. (scimage.cn)
  • The team has developed cutting-edge MRI technologies, which include a needleless method for myocardial ischemia detection named cardiac fMRI (cfMRI). (cedars-sinai.edu)
  • CK can also be elevated in the absence of neuromuscular diseases or cardiac injury, such as after strenuous exercise, intramuscular injection, and with renal disease. (medscape.com)
  • The elevated CK-BB in cerebrospinal fluid is a useful predictor of hypoxic brain injury after cardiac arrest. (medscape.com)
  • Such a series of destructive events has been implicated in diseases such as rheumatoid arthritis, myocardial infarction/reperfusion injury, atherogenesis, asthma, cystic fibrosis, emphysema, and vasculitis. (lu.se)
  • However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
  • Rationale: Both cardiomyocyte-restricted proteasome functional enhancement and pharmacological proteasome inhibition (PSMI) were shown to attenuate myocardial ischemia/reperfusion (I/R) injury. (elsevierpure.com)
  • Objectives: We sought to determine proteasome adequacy in I/R hearts, create a mouse model of cardiomyocyte-restricted PSMI (CR-PSMI), and test CR-PSMI impact on I/R injury. (elsevierpure.com)
  • siRNA-mediated management of myocardial ischemia reperfusion (IR) injury is greatly hampered by the inefficient myocardial enrichment and cardiomyocyte transfection. (scimage.cn)
  • MI with significant cardiomyocyte necrosis but without microvascular injury. (medscape.com)
  • Cardiomyocyte and microvascular necrosis leading to reperfusion hemorrhage. (medscape.com)
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
  • The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. (mdpi.com)
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • American College of Cardiology/American Heart Association/European Society of Cardiology/World Heart Federation Universal definition of myocardial infarction classification system and the risk of cardiovascular death: observations from the TRITON-TIMI 38 Trial (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis in Myocardial Infarction 38). (medscape.com)
  • Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
  • These data indicate that elevated levels of the MPO substrate SCN-, which can be readily modulated by dietary means, can protect against acute ischemia-reperfusion injury. (ku.dk)
  • Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
  • In patients with ST-segment elevation myocardial infarction (STEMI), ischemic postconditioning (iPOST) have shown ambiguous results in minimizing reperfusion injury. (lu.se)
  • Medical management of acute ST elevation myocardial infarction. (medscape.com)
  • 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. (medscape.com)
  • It has been reported that SIRT1/peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/nuclear factor erythroid-2-related factor 2 (Nrf2) signalling can mediate oxidative stress, which plays an important role in myocardial I/R injury ( 14 , 15 ). (spandidos-publications.com)
  • The main outcome was the size of the CMR-defined post-reperfusion infarct. (physiciansweekly.com)
  • We reported that there is infarct expansion after reperfusion, so once you open up the vessel, the heart attack actually gets larger. (medscape.com)
  • It was also reported that miR-132 was upregulated in simulated ischaemic injury in cultured hippocampal neurons ( 12 ). (spandidos-publications.com)
  • Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • Dive into the research topics of 'Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • The purpose of this study is to determine whether Glyceryl Trinitrate (GTN) reduces injury to the heart during heart-lung bypass surgery in combination with the newer technique of remote ischaemic preconditioning (RIPC). (druglib.com)
  • Remote ischaemic preconditioning (RIPC) has been shown to reduce perioperative myocardial injury (PMI) in patients having CABG even when cold blood cardioplegia or intermittent cross clamp fibrillation is used as cardioprotective measures. (druglib.com)
  • In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway. (spandidos-publications.com)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.com)
  • Our results indicate that estrogen plays a cardioprotective role in global myocardial ischemia-reperfusion injury in female rats. (illinois.edu)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • We investigated the effects of estrogen on global myocardial ischemia-reperfusion injury in rats that were ovariectomized (Ovx), sham-operated, or ovariectomized and then given 17β-estradiol (E 2 β) supplementation (Ovx+E 2 β). (illinois.edu)
  • Approach and Results - Rats underwent 30-minute ischemia per 24-hour reperfusion. (utmb.edu)
  • To evaluate the effects of dexmedetomidine on myocardial ischemia-reperfusion injury in rats and its anti-apoptotic role, as well as the mechanism by which it regulates Janus kinase 2/signal transducers and activators of transcription 3 signal. (ijpsonline.com)
  • Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
  • Conclusions - Ticagrelor, but not clopidogrel, administered just before reperfusion protects against reperfusion injury. (utmb.edu)
  • The needleless approach provides millions of patients with potential myocardial ischemic diseases a minimum risk solution for examining their coronary circulation without the potential harm from the standard clinical exams. (cedars-sinai.edu)
  • Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. (spandidos-publications.com)
  • Human HGF plasmid DNA therapy of cardiomyocytes is being examined as a potential treatment for coronary artery disease (a major cause of myocardial infarction (MI)), as well as treatment for the damage that occurs to the heart after MI. (wikipedia.org)
  • The increased production of HGF by transfected cardiomyocytes during injury has also shown to be a powerful chemo-attractant of adult mesenchymal stem cells via HGF/c-Met binding. (wikipedia.org)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • Methods and Results: Myocardial I/R were modeled by ligation (30 minutes) and subsequent release of the left anterior descending artery in mice overexpressing GFPdgn, a validated surrogate proteasome substrate. (elsevierpure.com)
  • Despite substantial declines in mortality following myocardial infarction (MI), subsequent left ventricular remodeling (LVRm) remains a significant long-term complication. (researchgate.net)
  • Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global mortality. (ku.dk)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • 1. MicroRNA-503 (miR-503) exacerbates myocardial ischemia/reperfusion (I/R) injury by inhibiting prosurvival signaling pathways, including PI3K/Akt and STAT3. (fullpicture.app)
  • An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. (jci.org)
  • Therefore, our aim was to develop a medium throughput comorbidity cell-based test system of myocardial I/R injury, hypercholesterolemia and hyperglycemia that mimics comorbidity conditions. (nih.gov)
  • The objectives of this study were to 1) determine the extent to which ascorbate or catechin alone at levels which could be in blood after dietary supplementation, can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic protective effect of ascorbate and catechin when given together. (usask.ca)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. (spandidos-publications.com)
  • However, despite numerous studies on myocardial I/R injury, deeper insight into the underlying mechanisms of myocardial I/R injury is needed. (spandidos-publications.com)
  • However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)
  • Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. (hindawi.com)
  • Mechanism investigations revealed a unique nuclear receptor subfamily 1 group D member 1/cardiotrophin-like cytokine factor 1 axis in the heart, which was critical in mediating the negative effects of shift work on myocardial damage. (physiciansweekly.com)
  • Ischaemia-reperfusion (I/R) injury is the most important and common cause of myocardial damage and subsequent heart failure worldwide ( 1 , 2 ). (spandidos-publications.com)
  • Interleukin-36 (IL-36), a newly discovered proinflammatory member of the IL-1 superfamily, may mediate this injury, but its role in the injured heart is currently not known. (jci.org)
  • In experimental groups A (n = 10) and B (n = 10), metabolic control of autoregulation was assessed by plots of myocardial oxygen consumption versus coronary flow generated by incremental increases in heart rate. (elsevierpure.com)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • If no injury or event is defined that could have led to a soft-tissue injury, the clinician should be reluctant to render a diagnosis of musculoskeletal chest pain. (medscape.com)
  • 2 ] hypothesised that the phosphatidylcholines are prime oxidising targets in the asthmatic airway based on their relative abundance, and that oxidised phosphatidylcholines (OxPC) are mechanistic effectors of oxidised stress in asthma, suggested by prior research demonstrating the ability of OxPC to perpetuate inflammation in ageing-related diseases, and their known causal role in both acute lung injury and acute respiratory distress syndrome [ 3 - 5 ]. (ersjournals.com)
  • Increased CK is predominantly used to diagnose neuromuscular diseases and acute myocardial infarction. (medscape.com)
  • this may be an important mechanism of decreased coronary perfusion and subsequent myocardial injury during reflow. (elsevierpure.com)
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Apparent histologic injury and elevated levels of serum myocardial enzymes and inflammatory factors were observed in the myocardial I/R model. (spandidos-publications.com)
  • and the increased morning levels of serum cortisol and plasma catecholamines leading to sympathetic overactivity, thereby resulting in increased myocardial demand. (medscape.com)
  • Determinants of collateral development in patients with acute myocardial infarction. (medscape.com)
  • The GRh2 pre‑treatment reduced the I/R‑ or H/R‑induced release of myocardial enzymes and the production of IL‑1β, IL‑18 and TNF‑α. (spandidos-publications.com)
  • Aborted MI (no or minimal myocardial necrosis). (medscape.com)
  • 3. Agomir-503 treatment worsens hypoxia/reoxygenation-induced injuries, while antagomir-503 treatment attenuates them and increases phosphorylation of Stat3 (Y705) and Akt (T450). (fullpicture.app)
  • miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
  • Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)
  • At 24 hours of reperfusion, myocardial proteasome activities were significantly lower whereas total ubiquitin conjugates and GFPdgn protein levels were markedly higher in all regions of the I/R hearts than the sham controls, indicative of proteasome functional insufficiency. (elsevierpure.com)
  • A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. (spandidos-publications.com)
  • A comparison of IR hearts with two controls, sham (perfused for a 15 min stabilization period) and continuous perfusion (perfused for 135 min), showed in most but not all measurements that this was a suitable model of IR injury. (usask.ca)
  • Although the mechanism remains elusive, the interest in exploring the therapeutic potential of MSC-Exo has greatly increased after the first report of MSC-Exo ameliorating myocardial ischemia/reperfusion injury in a mouse model 10 . (nature.com)
  • The left anterior descending coronary artery was ligated to construct the model of myocardial ischemia-reperfusion. (ijpsonline.com)