Association between preference for sweets and excessive alcohol intake: a review of animal and human studies. (1/53)

This report reviews a series of studies demonstrating a relationship between the consumption of sweets and alcohol consumption. There is consistent evidence linking the consumption of sweets to alcohol intake in both animals and humans, and there are indications that this relationship may be at least partially genetic in nature. Alcohol-preferring rats have a tendency to consume sucrose and saccharin solutions far beyond the limits of their normal fluid intake and this has been proposed to be a model of the clinical phenomenon known as loss of control. Furthermore, rats and mice, genetically bred to prefer alcohol, tend to choose more concentrated sweet solutions, compared to animals which do not prefer alcohol. Similar tendencies to prefer ultra-sweet solutions have been noted in studies of alcoholic subjects, with most alcoholics preferring sweeter sucrose solutions than do controls. Evidence also exists that those alcoholics who prefer sweeter solutions may represent a familial form of alcoholism. Finally, consumption of sweets and/or sweet solutions may significantly suppress alcohol intake in both animals and in alcoholics. Carbohydrate structure and sweet taste may contribute to this effect through different physiological mechanisms involving serotonergic, opioid, and dopaminergic functions. The possibility that there is concordance between sweet liking and alcohol consumption and/or alcoholism has theoretical, biological, and diagnostic/practical implications.  (+info)

Renomedullary and intestinal hyaluronan content during body water excess: a study in rats and gerbils. (2/53)

Our previous studies in rats have suggested a role for renomedullary hyaluronan (HA) in water homeostasis. The gerbil is known for its unique ability to conserve water. In the present study renal papillary and intestinal HA were compared between groups of anaesthetized gerbils and rats before and after up to 6 h of I.V. water loading. Baseline papillary HA in gerbils was only 37 % of that in the rat. Water loading in rats increased the papillary HA content. Elevation was maximal (+27 %, P < 0.05) after 2 h of water loading and then declined to control levels after 6 h of water loading (+3 %, n.s.). In contrast, the gerbil responded with a decreased papillary HA content during water loading. The depression was maximal after 2 h (-49 %, P < 0.05) and was still 41 % below the control values after 6 h (P < 0.05). The urine flow rate increased rapidly in the rat and its maximum, 21 times above the control level (P < 0.05), occurred at the HA peak, i.e. after 2 h of water loading while in the gerbil, the urine flow rate increased slowly and slightly and was only six times above control values after 6 h of water loading (P < 0.05). The HA content along the intestine was similar in the two species: lowest in the duodenum and jejunum and highest in the distal colon. To conclude, in the rat, the elevation of papillary interstitial HA during acute water loading would counteract water reabsorption by changing the physico-chemical characteristics of the interstitial matrix favouring rapid water diuresis. This would work as a complement to the powerful regulation by ADH. The gerbil has a diametrically different regulation of papillary HA turnover during water loading. The decreased papillary HA level during water loading and the slow and small diuretic response may represent a genetic difference in adaptation to enhance the ability to conserve water in an arid environment.  (+info)

Further characterization of the natriuretic factor derived from kidney tissue of volume-expanded rats. Effects on short-circuit current and sodium-potassium-adenosine triphosphatase activity. (3/53)

Boiled homogenates of kidneys from volume-expanded and hydropenic rats were subjected to column chromatography. The fraction eluting within the range of partition coefficients (Kav) 0.76-0.89 (fraction III) was lyophilized and the effects of this semipurified preparation were assessed on short-circuit current (SCC) across isolated frog skin, on rat kidney cortex Na-K-ATPase activity, and on sodium excretion by the rat in vivo. At a dose of 500 mug/ml, fraction III from expanded rat kidney inhibited SCC by 21 +/- 5% (P less than 0.01), whereas the same fraction from hydropenic rat kidney produced an insignificant change in SCC of 2 +/- 8 %. In a dose-response study, 50, 150, 500, and 1,500 mug/ml of fraction III from expanded rat kidney inhibited SCC by 4, 8, 19, and 28%, respectively; 500, 1,000 and 1,500 mug/ml inhibited Na-K-ATPase activity by 11, 22, and 49%, respectively. An identical study with fraction III from hydropenic animals showed no significant effect in either assay. Also, fractions from expanded and hydropenic rats, eluted after fraction III (fractions IV and V), had no effect on SCC or Na-K-ATPase activity. Fraction III also produced significant natriuresis in vivo at a dose of 500 mug/ml, confirming our observations that a natriuretic principle may be recovered from the kidneys of volume-expanded rats. We suggest that this natriuretic principle may act by reducing active sodium transport via inhibition of Na-K-ATPase.  (+info)

Early diagnosis of central pontine myelinolysis with diffusion-weighted imaging. (4/53)

Central pontine myelinolysis (CPM) occurs in the setting of rapidly corrected hyponatremia, especially in chronically debilitated patients. Conventional CT and MR imaging findings lag the clinical manifestations of CPM. We present a case in which restricted diffusion was identified within the central pons by using MR diffusion-weighted imaging within 24 hours of onset of patient tetraplegia and before findings were conspicuous with conventional MR imaging sequences (T1, T2, and fluid-attenuated inversion recovery).  (+info)

Urinary excretion half life of trichloroacetic acid as a biomarker of exposure to chlorinated drinking water disinfection by-products. (5/53)

AIMS: To measure accurately urinary elimination half life of trichloroacetic acid (TCAA). METHODS: A longitudinal pilot exposure/intervention study measured the elimination half life of TCAA in urine. Beverage consumption was limited to a public water supply and bottled water of known TCAA concentration, and ingestion volume was managed. The five participants limited fluid consumption to only the water provided. Consumption journals were kept by each participant and their daily first morning urine (FMU) samples were analysed for TCAA and creatinine. TCAA elimination half life curves were generated from a two week washout period using TCAA-free bottled water. RESULTS: Individual elimination half lives ranged from 2.1 to 6.3 days, for single compartment exponential decay, the model which fit the data. CONCLUSION: Urinary TCAA is persistent enough to be viable as a biomarker of medium term (days) exposure to drinking water TCAA ingestion within a range of realistic concentrations.  (+info)

The dipsomania of great distance: water intoxication in an Ironman triathlete. (6/53)

Of 371 athletes (62% of all finishers) whose weights were measured before and after the 226 km South African Ironman Triathlon, the athlete who gained the most weight (3.6 kg) during the race was the only competitor to develop symptomatic hyponatraemia. During recovery, he excreted an excess of 4.6 litres of urine. This case report again confirms that symptomatic hyponatraemia is caused by considerable fluid overload independent of appreciable NaCl losses. Hence prevention of the condition requires that athletes be warned not to drink excessively large volumes of fluid (dipsomania) during very prolonged exercise. This case report also shows that there is a delayed diuresis in this condition and that it is not caused by renal failure.  (+info)

In vivo measurement of brain extracellular space diffusion by cortical surface photobleaching. (7/53)

Molecular diffusion in the brain extracellular space (ECS) is an important determinant of neural function. We developed a brain surface photobleaching method to measure the diffusion of fluorescently labeled macromolecules in the ECS of the cerebral cortex. The ECS in mouse brain was labeled by exposure of the intact dura to fluorescein-dextrans (M(r) 4, 70, and 500 kDa). Fluorescein-dextran diffusion, detected by fluorescence recovery after laser-induced cortical photobleaching using confocal optics, was slowed approximately threefold in the brain ECS relative to solution. Cytotoxic brain edema (produced by water intoxication) or seizure activity (produced by convulsants) slowed diffusion by >10-fold and created dead-space microdomains in which free diffusion was prevented. The hindrance to diffusion was greater for the larger fluorescein-dextrans. Interestingly, slowed ECS diffusion preceded electroencephalographic seizure activity. In contrast to the slowed diffusion produced by brain edema and seizure activity, diffusion in the ECS was faster in mice lacking aquaporin-4 (AQP4), an astroglial water channel that facilitates fluid movement between cells and the ECS. Our results establish a minimally invasive method to quantify diffusion in the brain ECS in vivo, revealing stimulus-induced changes in molecular diffusion in the ECS with unprecedented spatial and temporal resolution. The in vivo mouse data provide evidence for: (1) dead-space ECS microdomains after brain swelling; (2) slowed molecular diffusion in the ECS as an early predictor of impending seizure activity; and (3) a novel role for AQP4 as a regulator of brain ECS.  (+info)

Crisis management during anaesthesia: water intoxication. (8/53)

BACKGROUND: Irrigation of closed body spaces may lead to substantial perioperative fluid and electrolyte shifts. A syndrome occurring during transurethral resection of prostate (TURP), and a similar syndrome described in women undergoing transcervical endometrial ablation (TCEA) are both characterised by a spectrum of symptoms which may range from asymptomatic hyponatraemia to convulsions, coma, and death. Such potentially serious consequences require prompt recognition and appropriate management of this "water intoxication" syndrome. OBJECTIVES: To examine the role of a previously described core algorithm "COVER ABCD-A SWIFT CHECK", supplemented by a specific sub-algorithm for water intoxication, in the management of this syndrome occurring in association with anaesthesia. METHODS: The potential performance of this structured approach for each of the relevant incidents among the first 4000 reported to the Australian Incident Monitoring Study (AIMS) was compared with the actual management as reported by the anaesthetists involved. RESULTS: From the first 4000 incidents reported to AIMS, 10 reports of water intoxication were identified, two from endometrial ablations under general anaesthesia and eight from male urological procedures under spinal anaesthesia. The "core" crisis management algorithm detected a problem in seven cases; however, it was deficient in dealing with neurological presentations. Diagnosis of the cause of the incident would have required a specific water intoxication sub-algorithm in eight cases and a hypotension algorithm in a further two cases. Corrective strategies also required a specific sub-algorithm in eight cases, while the hypotension and cardiac arrest sub-algorithms were required in conjunction with the water intoxication sub-algorithm in the remaining two. CONCLUSION: This relatively uncommon problem is managed poorly using the "core" crisis management sub-algorithm and requires a simple specific sub-algorithm for water intoxication.  (+info)

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