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Several techniques for developing incomplete obstruction of the common bile duct have been described but none of them properly represents a compression or constriction of the bile duct. In this study, a mild stenosis of the common bile duct was achieved in the rat by means of a double ligature including a cannula that could be easily slipped out of the ligatures. Sham-operated rats were used as controls. The studies, performed 7-10 days postoperatively, indicated that in ligated rats a duct constriction was produced, made evident by an increase of the biliary pressure, an upstream dilatation of the bile duct, an increase of the liver volume constituted by portal tracts, and ductular proliferation. Serum parameters were practically similar in ligated and control rats, except for a slight increase in serum bilirubin. Following intravenous injection of sodium taurocholate there were rapid increases of bile flow and bile salt output in both groups, but choleresis induced by sodium taurocholate was higher in ligated rats than in controls. The clearances of [14C]erythritol and [14C]sucrose suggested that ductular water contributing to bile flow and changes in biliary permeability were not involved in ligated rats. The limited repercussion of humoral effects and hepatic behaviour seen in ligated rats despite the morphological alterations induced make the mild stenosis of the bile duct a good model for the study of early stages of compression or constriction of the biliary tract.

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Adaptive hepatic changes were investigated in rats with mild stenosis of the common bile duct and in sham-operated controls. The studies were performed 24 h and 7-12 days postoperatively. A continuous intravenous infusion of taurocholic acid at stepwise-increasing rates was performed to explore the responses to bile acid effects. During the infusion, bile flow and the outputs of bile acids, phospholipids, cholesterol, alkaline phosphatase and gamma glutamyl transpeptidase were studied. At the end of the infusion, hepatic morphometric measurements were performed. In other experimental sets, biliary excretions of horseradish peroxidase, a marker of microtubule-dependent vesicular transport in the hepatocyte, and sulphobromophthalein, a well-known organic anion model, were studied. In other rats, bile acid pool size and composition were determined by depletion of bile. The results in rats with mild stenosis maintained for 24 h showed a greater susceptibility to the toxicity of taurocholic acid, as revealed by the abrupt decrement in bile flow at high rates of infusion, and increased outputs of phospholipids and canalicular enzymes. Conversely, rats with mild stenosis maintained for 7-12 days showed decreased bile acid maximum secretory rate and biliary outputs of phospholipids and canalicular enzymes, as well as hepatocyte hypertrophy. These findings may explain the limited hepatic and systemic repercussion of experimental mild stenosis of the common bile duct and help us to understand the early stages of constriction of the common bile duct in man.