title: [An increase of choleresis in secondary biliary cirrhosis in rats is caused by bile duct secretion].
abstract: Bile flow may be considerably increased in human cirrhosis. The mechanism of this increase has not been established. Two mechanisms have been proposed: a) increased canalicular filtration because of sinusoidal hypertension, or b) secretion by proliferated bile ductules. To distinguish between these two possibilities, we examined the determinants of bile secretion in rats with secondary biliary cirrhosis after bile duct obstruction. Sham-operated animals served as controls. Four weeks after bile duct ligation, all animals had cirrhosis. Bile flow was significantly higher and bile salt secretion significantly lower in cirrhotic animals than in controls. Biliary bicarbonate concentration was significantly higher in cirrhotic animals than in controls. Bile-to-plasma concentration ratio of erythritol was significantly lower in cirrhotic animals than in controls, suggesting a dilution of erythritol by a secretion distal to bile canaliculi. Bile-to-plasma ratio of sucrose was not significantly different in cirrhotics and controls, suggesting that paracellular permeability was not modified. Secretin, at the dose of 3 clinical units/100 g, induced an increase of approximately 75 percent in bile flow, and 70 percent in biliary bicarbonate concentration in cirrhotics. In conclusion, bile flow was increased in biliary cirrhosis in rats. The dilution of erythritol, the increase in biliary bicarbonate concentration and the increased response to secretin strongly suggest that increased choleresis was due, at least in part, to secretion by bile ductules or ducts. These results confirm that secondary biliary cirrhosis is a good experimental model for the study of alterations of bile secretion in cirrhosis.
authors.affiliation: Unité de Recherches de Physiopathologie Hépatique, INSERM U-24, Hôpital Beaujon, Clichy.
authors.forename: J
authors.initials: J
authors.lastname: Taillandier
authors.forename: M
authors.initials: M
authors.lastname: Dumont
authors.forename: V
authors.initials: V
authors.lastname: Mesa
authors.forename: C
authors.initials: C
authors.lastname: Degott
authors.forename: S
authors.initials: S
authors.lastname: Erlinger
mesh_terms: D000818:Animals; D001646:Bile / Q000378:metabolism*; D001647:Bile Acids and Salts / Q000378:metabolism; D001648:Bile Canaliculi / Q000378:metabolism; D001652:Bile Ducts / Q000378:metabolism*; D004195:Disease Models, Animal; D004573:Electrolytes / Q000032:analysis; D004896:Erythritol; D008105:Liver Cirrhosis, Biliary / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012633:Secretin / Q000008:administration & dosage; D013395:Sucrose
chemical_list: D001647:Bile Acids and Salts; D004573:Electrolytes; D012633:Secretin; D013395:Sucrose; D004896:Erythritol
vernacular_title: L'augmentation de la cholérèse au cours de la cirrhose biliaire secondaire chez le rat est due à une sécrétion par les voies biliaires.