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Research has been conducted on interhapatic cholestiasis of pregnancy. The authors have tested the hypothesis that during this disease bile acid activates the myometrial oxytocin receptor pathway, and they present the results.

Heal water and electrolyte absorption exceed jejunal absorption in both the basal and meal-stimulated states. The purposes of these experiments were to determine: (1) if luminal bile acids alter basal or meal-stimulated intestinal absorption, and (2) if there is site specificity or meal stimulation of intestinal bile acid absorption. Twenty-five centimeters of canine proximal jejunal and distal flea1 Thiry-Vella fistnlas were constructed. Simultaneous jejunal and ileal absorption studies (n = 88 ) were performed with a luminal perfusate containing pelyethylene glyeol labeled with radioactive carbon-14 to calculate the absorption of water, electrolytes, and the bile acid tauroeholate (TC). In group 1, there was no TC in the lumma1 perfusate, whereas in group 2, 1 O mM of TC was present in the 1uminal perfusate. Half of the observations were performed after a meal stimulus, which consisted of an orally ingested, 480-kcal mixed nutrient meal. Intraluminal TC did not affect basal or mealstimulated water or electrolyte absorption. in both the basal and meal-stimulated states, ileal absorption of water, electrolytes, and TC significantly exceeded jejunal absorption (p Intraluminal TC does not alter basal or mealstimulated intestinal water and electrolyte absorption. A meal stimulates increased water and electrolyte absorption in both the jejanum and the ileum, but it stimulates bile acid absorption in the ileum only. Bile acid absorption is site specific and responsive to a meal stimulus.

Veterans are frequently older, have more chronic illnesses, and take more medications than subjects volunteering for clinical trials. Because these factors may impair the effectiveness of lipid-lowering drug therapy, the effectiveness of drag therapy in veterans may differ from that measured in randomized controlled trials. In 297 patients with type IIa hyperlipidemia attending a large Veterans Administration Medical Center lipid clinic, adverse effects, compliance, lipid and lipoprotein responses to drug therapy were prospectively monitored. Bile acid sequestrants (4 packets/day) were associated with a high rate of adverse effects, and had the highest drug discontinuance rate (37%) and poorest compliance (73 [+ or-] 3% of the doses prescribed reported ingested) of all agents. Patients aged >60 years tolerated therapy with bile acid sequestrants less well than did younger veterans (p (Am J Cardiol 1993;71:759-765)

Pretreatment with the mild irritant 1 mmol acidified taurocholate protects the gastric mucosa from the injury induced by the subsequent application of 5 mmol acidified taurocholate, a phenomenon referred to as 'adaptive cytoprotection.' How this occurs remains an enigma. The purpose of this study was to investigate the role of sensory neurons and mucus secretion in this phenomenon. Prior to injury with 5 mmol acidified taurocholate (pH 1.2), the stomachs of six groups of rats were subjected to the following protocol. Two groups were topically pretreated with either saline or the mild irritant I mmol acidified taurocholate. Two other groups received the topical anesthetic 1% lidocaine prior to pretreatment with either saline or 1 mmol acidified taurocholate. The last two groups, got the mucolytic agent 10% N-acetyleysteine (NAC) after pretreatment with either saline or 1 mmol acidified taurocholate. Injury was assessed by measuring net trammucosal ion fluxes, luminal appearance of deoxyribonucleic acid (DNA), and gross and histologic injury. Pretreatment with the mild irritant 1 mmol acidified taurocholate significantly decreased bile acid-induced luminal ion fluxes and DNA accumulation, suggesting mucosal protection (corroborated by gross and histologic injury analysis). This effect was negated by lidocaine but not by NAC. Thus, it appears that sensory neurons, and not increased mucus secretion, play a critical role in adaptive cytoprotection.

Duodenogastric reflux (backflow of the contents of the first portion of the small intestine into the stomach) is known to occur as a complication following gastric (stomach) surgery. It has been suggested that duodenogastric reflux (DGR) may also be implicated in the development of gastric symptoms following cholecystectomy (surgical removal of the gallbladder). A study was undertaken to determine the extent of DGR in 15 patients with gallstones who underwent cholecystectomy; specimens of stomach juice were obtained before and after surgery and the bile acid content of the DGR was quantified. These results were compared with results obtained from a group of healthy control subjects. The average bile acid concentration for the control subjects was 2.25 micromoles reflux/hour, compared with 8.86 for the patient group before cholecystectomy and 24.55 for patients following surgery. No bile acid was found in either the before- or after-surgery specimens of five of the 15 surgery patients. A significant increase in bile acid was found in the remaining 10 surgical patients (67 percent). It is concluded that gallstone disease is not always associated with duodenogastric reflux; however, when it does occur, the level is higher than that of control subjects and the level increases significantly following cholecystectomy. This finding may explain some of the stomach symptoms associated with gallbladder disease, and post-cholecystectomy syndrome may be due in part to the increase in DGR. (Consumer Summary produced by Reliance Medical Information, Inc.)