Effect of somatostatin on determinants of bile flow in unanesthetized dogs.

Seven dogs each underwent cholecystectomy, ligation of the accessory pancreatic duct, and insertion of a Thomas duodenal cannula opposite the ampulla of Vater. After full recovery, bile secretions were studied in the unanesthetized dogs by opening the cannula and placing a ureteric catheter through the papilla into the common bile duct. All animals received, throughout study, constant infusions of taurocholic acid to replace losses caused by interruption of the enterohepatic circulation and 14 C-erythritol for measurement of erythritol clearance. After bile flow stabilized somatostatin 800 ng/kg/minute was infused for 100 minutes and bile flow declined from 3.0 +/- 0.7 ml/10 minutes (SD) to 1.19 +/- 0.47 ml/10 minutes (p less than 0.001) and 14C-erythritol clearance fell from 3.6 +/- 1.14 to 1.77 +/- 0.43 ml/10 minutes (p less than 0.001). Bile salt output was unchanged, indicating that somatostatin inhibited bile salt-independent canalicular flow (BSICF). In other experiments animals underwent intraduodenal acidification which resulted in a marked increase in bile flow. Somatostatin infusion again causes a sharp fall in bile flow (p less than 0.05) suggesting that somatostatin also inhibited ductular flow. Infusion of somatostatin did not inhibit choleresis produced by exogenous secretin administration. Thus, somatostatin inhibits 1) ductular flow by inhibiting secretin release and 2) BSICF by a direct effect or by decreasing the release of hormones which induce canalicular flow.