Transport of fluid and biliary lipids in the canine gallbladder in experimental cholecystitis

Svanvik, Joar; Allen, Bruce G.; Bernhoft, Robin A.; Way, Lawrence W.

doi:10.1016/0022-4804(86)90057-0

Cited by 22 publications

(15 citation statements)

References 17 publications

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“…The secreting function of guinea pig gallbladder epithelium is stimulated by an increase in the intracellular cAMP level (6), and seems to prevail during digestion or in cholecystitis (3,7,8). Under secreting conditions, not only is Na ϩ absorption inhibited due to inhibition of the apical Na ϩ /H ϩ antiporter; in addition, both Cl Ϫ /HCO 3 Ϫ exchange and conductance for Cl Ϫ and HCO 3 Ϫ (the latter being able to determine a net HCO 3 Ϫ electrogenic secretion) are apically enhanced (6,9).…”

mentioning

confidence: 99%

An Anion Channel in Guinea Pig Gallbladder Epithelial Cells Is Highly Permeable to HCO−3

Meyer

Garavaglia

Bazzini

et al. 2000

Biochemical and Biophysical Research Communications

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mentioning

confidence: 99%

An Anion Channel in Guinea Pig Gallbladder Epithelial Cells Is Highly Permeable to HCO−3

Meyer

Garavaglia

Bazzini

et al. 2000

Biochemical and Biophysical Research Communications

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“…In guinea pigs, acute cholecystitis is accompanied by an increased absorption of conjugated bile acids (27). In cholecystitis induced in dogs by ligating the cystic duct, a net absorption of fluids, bile acids, cholesterol, and phospholipids occurred during the first 24-48 hr after ligation (30). In cholesterolosis of the gallbladder in humans, free cholesterol is present in large quantities in epithelial cells (20) and an increase in free and esterified cholesterol and triglycerides has been measured in the mucosa (15,34).…”

Section: Semmentioning

confidence: 99%

“…In the pathogenesis of acute acalculous cholecystitis experimentally induced in dogs by ischemia and reperfusion, the roles of microcirculatory disturbances, free radicals, and membrane-bound phospholipases have recently been highlighted (33). Administration of aspirin and indomethacin during experimental cholecystitis resulted in a decreased rate of fluid secretion into the gallbladder lumen in dogs (30) and reversed the gallbladder secretion into a net absorption in cats (31 …”

Section: Semmentioning

confidence: 99%

Lipidosis Induced in the Dog Gallbladder by a Direct 5-Lipoxygenase Inhibitor

et al. 1996

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“…Cystic duct ligation in prairie dogs does not cause cholecystitis unless concentrated bile is injected in obstructed gallbladders . Daily infusions of sterile fresh bile introduced into gallbladders of domestic dogs are necessary to cause a similar effect . In contrast, severe acute cholecystitis develops quickly in untreated guinea pigs 3 days following ligation of the common bile duct .…”

Section: Introductionmentioning

confidence: 99%

Roles of cholesterol and bile salts in the pathogenesis of gallbladder hypomotility and inflammation: cholecystitis is not caused by cystic duct obstruction

Behar

2013

Neurogastroenterology Motil

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A large number of human and animal studies have challenged the hypothesis that cystic duct obstruction by gallstones causes cholecystitis. These studies suggest that lithogenic bile that can deliver high cholesterol concentrations to the gallbladder wall causes hypomotility and creates a permissive environment that allows normal concentrations of hydrophobic bile salts to inflame the mucosa and impair muscle function inhibiting gallbladder emptying. High concentrations of cholesterol increase its diffusion rates through the gallbladder wall where they are incorporated into the sarcolemmae of muscle cells by caveolin proteins. High caveolar cholesterol levels inhibit tyrosine-induced phosphorylation of caveolin proteins required to transfer receptor-G protein complexes into recycling endosomes. The sequestration of these receptor-G protein complexes in the caveolae results in fewer receptors recycling to the sarcolemmae to be available for agonist binding. Lower internalization and recycling of CCK-1 and other receptors involved in muscle contraction explain gallbladder hypomotility. PGE2 receptors involved in cytoprotection are similarly affected. Cells with a defective cytoprotection failed to inactivate free radicals induced by normal concentrations of hydrophobic bile salts resulting in chronic inflammation that may lead to acute inflammation. Ursodeoxycholic acid salts (URSO) block these bile salts effects thereby preventing the generation of free radicals in muscle cells in vitro and development of cholecystitis in the ligated common bile duct in guinea pigs in vivo. Treatment with URSO improves muscle contraction and reduces the oxidative stress in patients with symptomatic cholesterol gallstones by lowering cholesterol concentrations and blocking the effects of hydrophobic bile salts on gallbladder tissues.

show abstract

Transport of fluid and biliary lipids in the canine gallbladder in experimental cholecystitis

Cited by 22 publications

References 17 publications

An Anion Channel in Guinea Pig Gallbladder Epithelial Cells Is Highly Permeable to HCO−3

An Anion Channel in Guinea Pig Gallbladder Epithelial Cells Is Highly Permeable to HCO−3

Lipidosis Induced in the Dog Gallbladder by a Direct 5-Lipoxygenase Inhibitor

Roles of cholesterol and bile salts in the pathogenesis of gallbladder hypomotility and inflammation: cholecystitis is not caused by cystic duct obstruction

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