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Query: UMLS:C0008325 (cholecystitis)
 3,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the mechanism of concentration of bile, the normal canine gallbladders were cannulated through the cystic duct into the gallbladder neck with polyethylene tube, and hypotonic, isotonic and hypertonic salines as well as hepatic and gallbladder biles were placed in the gallbladder. Low molecular electrolytes such as Na+ and Cl- were transported across the epithelial membrane against water flux. The hepatic bile was decreased markedly in volume and each level of electrolytes including bile acids approached that in the gallbladder bile. The different results were obtained by concentration of the hepatic bile in the gallbladder with chemically induced cholecystitis.
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PMID:A new approach to absorptive function of gallbladder. 66 94

Nine hundred ninety-two consecutive patients with cholelithiasis and cholecystitis are reported on. In Finland, these diseases seem to affect women more often than men as only 18% in the present series were men. The frequency of these diseases increases with advancing age and reaches its peak in patients sixty to sixty-five years of age. Therapy always consisted of cholecystectomy. The incidence of minor technical complications varied from 1.1% in group I to 4.5% in group III (6.1% in group IIB). Postoperative nonfatal complications varied from 2.0% in group I to 5.2% in group III (8.1% in group IIB). The age-adjusted duration of postoperative hospitalization was about eight days (in group IIB, nine days. In groups I and II one patient died whereas in group III two died. The mortality varied from 0.2% in group I to 0.6% in group III (1.2% in group IIB). The overall mortality for this series was 0.5%. On the basis of this analysis and the good results, I have concluded that cholecystectomy is the preferred therapy for cholecystitis at all stages when all coexisting diseases and water and elctrolyte imbalances have been treated.
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PMID:Treatment of cholecystitis: cholecystostomy or cholecystectomy? 95 39

Intake of naftusia mineral water influences insulin, glucagon and gastrin secretion measured in patients with chronic acalculous cholecystitis in the following manner: initial low insulin and glucagon, normal gastrin levels rise; initial elevated gastrin and normal glucagon lower at the start of the treatment. The course of naftusia crenotherapy resulted in adaptation to water intake as evidenced by normalization of high gastrin, low glucagon levels in minimal rise of insulin.
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PMID:[The effect of a course of naftusia water intake on the gastroenteropancreatic endocrine system]. 192 98

Changes in biochemical bile composition were investigated in 42 patients with chronic infective acalculous cholecystitis on combined sanatorium treatment. In those with carbohydrate dysbolism, bile production was found inhibited possibly due to the intake of carbonate sodium mineral water of moderate mineralization containing bromine and fluorine with high concentrations of bromine, in particular.
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PMID:[The characteristics of using mineral waters with an increased boron content in rehabilitating patients with hepatobiliary pathology]. 192 99

A case of acute acalculous cholecystitis in a two year-old girl that undergone drowning in sweet water is reported. Cerebral death was diagnosed and the organs donation was authorized. A biliary peritonitis secondary to gallbladder perforation was met during organs extraction. The liver was rejected.
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PMID:[Acute acalculous cholecystitis secondary to immersion asphyxia. Implications in organ donation]. 193 97

Naturally occurring ulcerative cholecystitis was present in a flock of 21-day-old turkey hens that were accidentally given at least 0.004% 3-nitro-4-hydroxy-phenylarsonic acid (3-NITRO) in their water for 2 days. Similar lesions were reproduced by administering 0.002% 3-NITRO to 2-day-old turkey poults for 6 days. Turkeys 31 days old were given up to 0.004% 3-NITRO in their water for 6 days, but no gall bladder ulcers were present in these poults. The toxicity to turkeys of 3-NITRO in the water appears to be age-dependent.
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PMID:Ulcerative cholecystitis produced by 3-nitro-4-hydroxy-phenylarsonic acid toxicosis in turkey poults. 202 59

Gallbladder tissue from patients with acute acalculous cholecystitis contains increased amounts of prostanoids when compared to normal gallbladder tissue. Platelet-activating factor (PAF) is a potent stimulus of eicosanoid formation. It has been implicated as a mediator of acute inflammatory processes and systemic responses to shock. In this study the role of PAF in acute acalculous cholecystitis was evaluated. Anesthetized cats underwent gallbladder perfusion with a physiologic buffer solution containing [14C]polyethylene glycol as a nonabsorbable tracer to quantitate mucosal water absorption. Platelet-activating factor was infused into the hepatic artery for 2 hours. Control experiments were performed when vehicle alone was infused. Experiments also were performed when indomethacin was administered intravenously and when indomethacin and PAF were administered. Gallbladder mucosal absorption/secretion and perfusate and tissue prostaglandin E (PGE) and 6 keto prostaglandin F1 alpha (6-keto PGF1 alpha) levels were evaluated. Gallbladder inflammation was evaluated by beta-glucuronidase and myeloperoxidase tissue concentrations and by a histologic scoring system. Platelet-activating factor eliminated gallbladder absorption and produced net fluid secretion associated with dose-related increases in perfusate PGE concentrations and gallbladder tissue PGE and 6 keto PGF1 alpha levels when compared to control values. Platelet-activating factor produced significant inflammation in the gallbladder with increases in the histologic score of inflammation and tissue lysosomal enzyme activities. Indomethacin significantly decreased the fluid secretion, prostanoid levels, and inflammation produced by PAF. The results suggest that PAF may induce acute gallbladder inflammation associated with systemic stress through a prostanoid-mediated mechanism.
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PMID:The role of prostanoids in the production of acute acalculous cholecystitis by platelet-activating factor. 217 43

Current information suggests that arachidonic acid metabolites are involved in the development of cholecystitis. The purpose of this study was to evaluate eicosanoid formation during the development of experimental cholecystitis in cats. Lysophosphatidylcholine is found in the gallbladders of patients with cholecystitis and is known to be a cytolytic, membrane-damaging substance. Anesthetized cats underwent gallbladder perfusion with and without 1.5 mmol/L lysophosphatidylcholine. Additional experiments were performed when calcium ionophore were added to the perfusates and experiments were performed when cats were treated with indomethacin and underwent perfusion with lysophosphatidylcholine. Changes in the gallbladder were determined by evaluating mucosal water transport as measured by determining the changes in concentration in a nonabsorbable marker, by protein secretion and by beta-glucuronidase accumulation in gallbladder tissue as an index of inflammation. Eicosanoid formation was evaluated by measuring perfusate concentrations and gallbladder homogenate concentrations by radioimmunoassay of prostaglandin E, 6 keto prostaglandin F1 alpha, leukotriene B4 and leukotriene C4. Lysophosphatidylcholine perfusion reversed the control patterns of absorption and produced water exsorption, produced an efflux of protein into the perfusate and increased beta-glucuronidase activity. These changes were accompanied by increased production of prostaglandin E and 6 keto prostaglandin F1 alpha in gallbladder perfusate and homogenate. The concentration of leukotriene C4 in gallbladder effusate was increased by lysophosphatidylcholine when compared with control values. Indomethacin inhibited the protein efflux, decreased beta-glucuronidase levels and decreased prostaglandin E and 6 keto prostaglandin F1 alpha formation when compared with values produced by lysophosphatidylcholine alone. Cyclooxygenase inhibition did not alter the secretion of water into the gallbladder or perfusate leukotriene C4 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostanoids and leukotrienes in experimental feline cholecystitis. 236 79

Primary bacterial peritonitis and catheter-associated infections compose the large majority of abdominal events in continuous ambulatory peritoneal dialysis (CAPD) patients. Yet occasionally primary pathology involving the abdominal viscera develops, and surgery is frequently considered. The early manifestations of intraabdominal inflammation or bleeding in patients undergoing CAPD depend on the pathological process, its access to the peritoneal cavity, and whether generalized bacterial peritonitis supervenes to obscure helpful physical findings. Clear dialysate is not a reliable sign that major pathology is absent, nor does initial stabilization of the clinical course with antibiotic therapy uniformly indicate that surgery will not be necessary. Polymicrobial peritonitis may develop in cholecystitis, pancreatitis, or from a colonic source, the latter featuring more bacterial species and more gram-negative and anaerobic organisms. A history directed at progression of symptoms and sites of abdominal discomfort and an examination for deep local tenderness and bowel incarcerated in an abdominal wall hernia are essential. Measurement of dialysate amylase and Gram stain of dialysate for food fibers may be helpful. Imaging techniques such as abdominal radiographs for dilated bowel or free subdiaphragmatic air, ultrasonography of the gallbladder or pancreas, computed tomographic (CT) scanning of the lower abdomen, and water-soluble contrast colonic studies may help identify the pathologic process. Special studies such as these should be considered early in the course of suspected unusual abdominal events in patients on CAPD.
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PMID:Abdominal catastrophes and other unusual events in continuous ambulatory peritoneal dialysis patients. 236 12

Continuing evaluation of the pathophysiology of gallbladder disease has demonstrated significant relationships between gallbladder mucosal fluid transport, gallbladder inflammation, and prostanoid formation. Inflamed gallbladder mucosa secretes, rather than absorbs, fluid, a process associated with prostaglandin formation. Bradykinin has been previously implicated in the pathogenesis of cholecystitis and, in the intestine, bradykinin stimulates mucosal fluid secretion by a prostaglandin-mediated mechanism. Bradykinin was infused into the gallbladder lumen and administered intraarterially into the hepatic artery of perfused cat gallbladders. Both methods of bradykinin administration reversed the mucosal absorption present during control experiments as measured by concentration changes in a nonabsorbable marker. Perfusate and gallbladder tissue prostaglandin E concentrations were significantly increased by bradykinin when compared to control values. Concentrations of 6-keto PGF1 alpha in perfusate solutions and in gallbladder tissue were significantly increased, suggesting bradykinin increased prostacyclin formation. Bradykinin administration significantly increased inflammation, as evaluated by a histologic scoring system. Indomethacin was administered intravenously along with luminal perfusion of the gallbladder with bradykinin. Indomethacin significantly decreased gallbladder fluid secretion and prostanoid formation, but not histologic inflammation, when compared to values produced by bradykinin alone. An increase in systemic vascular and bile kinin concentrations produces gallbladder mucosal water secretion, a process which may be mediated by prostanoids. Histologic inflammation produced by bradykinin was not prevented by indomethacin.
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PMID:Effect of bradykinin on feline gallbladder water transport and prostanoid formation. 258 88


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