Prenatal sonographic features of spondylocostal dysostosis and diaphragmatic hernia in the first trimester. (1/60)

Spondylocostal dysostosis is a congenital disorder characterized by multiple malformations of the vertebrae and ribs. We describe the sonographic features of an affected fetus at 12 and 14 weeks of gestation. The fetus had thoracic scoliosis, multiple vertebral and rib malformations and a grossly dilated stomach that had herniated into the chest through a left-sided diaphragmatic hernia. The stomach spanned the whole length of the fetal trunk.  (+info)

Pseudoaffective cardioautonomic responses to gastric distension in rats. (2/60)

We examined the heart rate response to gastric distension, the involvement of vagal and sympathetic sensory afferents, adrenergic and cholinergic neural pathways, and the effects of capsaicin on this response in anesthetized rats. Gastric distension volume dependently decreased heart rate by 24.5% (resting rate = 219.87 +/- 14.06 beats/min, mean rate during gastric distension with 15 ml = 165.97 +/- 17.36 beats/min, P < 0.05). The bradycardic response was significantly decreased after removal of the celiac plexus (9.71 +/- 1.77 vs. 38.03 +/- 7.06% in controls, P < 0.05) or after bilateral subdiaphragmatic vagotomy (6.38 +/- 2.65%, P = 0.05). The response to gastric distension was largely prevented by systemic capsaicin (29.92 +/- 4.93% in controls, 2.58 +/- 4.19% after systemic capsaicin, P < 0.05) and decreased by perivagal capsaicin (18.72 +/- 4.75%, P < 0.05). Atropine almost completely prevented the cardiac response to distension, while propranolol and bretylium partially blocked it, implying the response is primarily mediated by cholinergic efferents but also involves adrenergic pathways. We conclude that unmyelinated, capsaicin-sensitive vagal afferents are essential to the pseudoaffective cardioautonomic response to a noxious gastric stimulus.  (+info)

Modulation by endogenous nitric oxide of acid secretion induced by gastric distention in rats: enhancement by nitric oxide synthase inhibitor. (3/60)

The mechanism underlying acid hypersecretion induced by gastric distention was investigated in rats, especially in relation to endogenous nitric oxide (NO). Under urethane anesthesia, rat stomach was distended by instillation of saline (1-10 ml) through the acute fistula that was provided through a pylorus. Gastric samples were collected every 1 h, and the acid secretion was measured by titration with 100 mM NaOH. Gastric acid secretion was increased by distention, and the degree of stimulation was dependent on the volume of saline instillation; a maximal response occurred with 6-ml instillation, which maintained the intraluminal pressure of about 20 cm H(2)O. The increased acid secretory response induced by distention was completely blocked by omeprazole and significantly mitigated by vagotomy, sensory deafferentation, atropine, or famotidine but markedly enhanced by the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). On the other hand, the enhanced acid response in the presence of L-NAME occurred in an L-arginine-sensitive manner and was almost totally abolished by vagotomy and sensory deafferentation as well as by atropine. Gastric distention increased the release of NO metabolites and histamine into the gastric lumen. The NO metabolite release in the distended stomach was significantly decreased by vagotomy or L-NAME, whereas the histamine output was decreased by vagotomy but increased by L-NAME in an L-arginine-sensitive manner, respectively. These results suggest that 1) gastric distention increases acid secretion, initially through the perception by sensory neurons of the mechanical stimulation and mainly through the efferent vagocholinergic pathway, with the process being modified by endogenous NO, and 2) this molecule, released in a vagal-dependent manner, exerts a negative influence on acid secretion, at least in part by suppressing histamine release from the histamine-containing cells.  (+info)

TNF-alpha activates solitary nucleus neurons responsive to gastric distension. (4/60)

Tumor necrosis factor-alpha (TNF-alpha) is liberated as part of the immune response to antigenic challenge, carcinogenesis, and radiation therapy. Previous studies have implicated elevated circulating levels of this cytokine in the gastric hypomotility associated with these disease states. Our earlier studies suggest that a site of action of TNF-alpha may be within the medullary dorsal vagal complex. In this study, we describe the role of TNF-alpha as a neuromodulator affecting neurons in the nucleus of the solitary tract that are involved in vago-vagal reflex control of gastric motility. The results presented herein suggest that TNF-alpha may induce a persistent gastric stasis by functioning as a hormone that modulates intrinsic vago-vagal reflex pathways during illness.  (+info)

Modulation of gastric distension-induced sensations by small intestinal receptors. (5/60)

Duodenal lipid exacerbates gastrointestinal sensations during gastric distension. Using luminal application of the local anesthetic benzocaine, we investigated the role of intestinal receptors in the induction of these sensations. Nine healthy subjects were studied on five occasions, during which isotonic saline or 20% lipid (2 kcal/min), combined with (duodenal or jejunal) 0.75% benzocaine or vehicle at 2.5 ml/min, was infused intraduodenally before and during gastric distension. Intragastric pressures and volumes, gastrointestinal sensations, and plasma CCK levels were determined. Duodenal lipid combined with vehicle increased gastric volume (in ml: saline, -10 +/- 18; lipid/vehicle, 237 +/- 30) and plasma CCK [mean levels (pmol/l): saline, 2.0 +/- 0. 2; lipid/vehicle, 8.0 +/- 1.6] and, during distensions, induced nausea (scores: saline, 3 +/- 2: lipid/vehicle, 58 +/- 19) and decreased pressures at which fullness and discomfort occurred. Duodenal but not jejunal benzocaine attenuated the effect of lipid on gastric volume, plasma CCK, and nausea during distension (135 +/- 38 and 216 +/- 40 ml, 4.6 +/- 0.6 pmol/l and not assessed, and 37 +/- 12 and 64 +/- 21 for lipid + duodenal benzocaine and lipid + jejunal benzocaine, respectively) and on pressures for sensations. In conclusion, intestinal receptors modulate gastrointestinal sensations associated with duodenal lipid and gastric distension. There is also the potential for local neural mechanisms to regulate CCK release and thereby reduce afferent activation indirectly.  (+info)

Acute gastric dilatation accompanied by diabetes mellitus. (6/60)

A 72-year-old man with diabetic triopathy was hospitalized with methicillin resistant staphylococcus aureus pneumonia. Six hours after the admission, his abdomen was fully expanded. An abdominal X-ray showed gastric dilatation. After insertion of a gastric tube to extract gastric air, his abdomen was flat and gastric dilatation improved. A positive Schellong test and decreased coefficient of RR interval in electrocardiogram variation indicated autonomic neuropathy, which may explain the reason for gastric hypomotility. Acute gastric dilatation in this patient may have occurred due to gastric hypomotility as a result of diabetic autonomic neuropathy in addition to gastric motility inhibition resulting from gastric autonomic nerve stimulation by bacterial toxin.  (+info)

Gastric rupture caused by acute gastric distention in non-neonatal children: clinical analysis of 3 cases. (7/60)

OBJECTIVE: To study gastric rupture, a progressive, rapid and high mortality condition, caused by acute gastric distention (GRAGD) and its appropriate diagnosis and treatment. METHODS: The etiology, pathology, clinical manifestations and experiences in 3 children with GRAGD were reviewed. RESULTS: Case 1: After diagnosing GRAGD and stabilizing her shock with massive fluid replacement, gastrostomy was performed. Her postoperative course was uneventful because of fasting, suction, fluid infusion, correction of acidosis and supporting nutrition. Case 2: After diagnosing gastric distention which subsided with conservative therapy for 9 days, she suddenly had gastric rupture when she had not eaten for 6 days. She died of shock and had no chance for surgery. Case 3: The patient had sudden abdominal pain, distention and vomiting with severe shock for 4 days. Emergency surgery found gastric rupture and the method was the same as Case 1. The patient survived but has brain impairment. Case 1 and 3 showed multifocal transmural necrosis. CONCLUSIONS: Symptoms like overeating, bulimia, changes in kind of food, X-ray showing large distended stomach and massive pneumoperitoneum were seen after gastric rupture and can help to diagnose this condition. Clinical course of gastric distention with toxic shock progresses rapidly, however subsequent gastric rupture exacerbates the shock and makes the treatment difficult treatment. It is extremely important that a laparotomy be performed at once after stabilizing shock with massive fluid replacement. Postoperative nutritional support and fluid replacement will increase survival. It is very important that when gastric distention disappears after conservative therapy, the doctor should assess carefully whether the gastric wall recovery is under way by using effective methods of examination.  (+info)

Reliability of epigastric auscultation to detect gastric insufflation. (8/60)

BACKGROUND: We studied the reliability of epigastric auscultation to detect gastric insufflation in 30 anaesthetized, paralysed intubated patients. METHODS: A 16FG gastric tube was positioned with the tip in the mid-oesophagus with the proximal end attached to an injection port with a one-way valve. Four observers participated in the study. Observers were paired and each pair studied 15 patients. Each patient underwent four test sequences in random order, two by each observer. Each test sequence comprised one observer injecting different volumes of air (0.25 ml, 0.5 ml, 1 ml, 2 ml, 3 ml, 4 ml, 5 ml, 10 ml, 15 ml and 0 ml as a control) in random order whilst the second blinded observer listened with a stethoscope over the epigastrium. Each randomized volume was injected rapidly at 5 s intervals for 1 min. The number of injections required to detect air entering the stomach was recorded. The stomach was deflated between each test sequence. RESULTS: To detect air entering the stomach with 95% confidence, 11 injections were required for 0.25 ml; 7 for 0.5 ml; 3 for 1 ml; 2 for 2 ml and 3 ml, and I for > or =4 ml. The mean (range) inter- and intraobserver reliability was 0.73 (0.71-0.75) and 0.76 (0.76-0.89), respectively. The incidence of false positives was 21% (25/120) and the incidence of false negatives was 10% (103/1080), making the specificity and sensitivity 79% and 91%, respectively. CONCLUSIONS: We conclude that epigastric auscultation can detect gastric insufflation of 0.25 ml air after 11 breaths and > or = 4 ml air after one breath with 95% confidence. Inter- and intraobserver reliability is moderate to excellent. Epigastric auscultation should be repeated to reduce the risk of false positives.  (+info)

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