Long-term administration of the somatostatin analogue, octreotide, is complicated by gallstone formation. Somatostatin is known to inhibit hepatic bile secretion and gallbladder emptying. However, the effect of octreotide on gallbladder bile composition remains unknown. Therefore, we tested the hypothesis that octretide would alter hepatic bile composition and cause gallbladder stasis, thereby increasing gallbladder bile solute concentrations. Fourteen control prairie dogs received daily saline injections, whereas 10 animals received 1-mu-g of octreotide subcutaneously three times per day for 5 days. Cholecystectomy and common bile duct cannulation were then performed. Octreotide increased hepatic bile concentrations of bilirubin monoglucuronide (p < 0.05), total bilirubin (p < 0.05), and total protein (p < 0.01). Rsa, an index of gallbladder stasis, was decreased (p < 0.01) in the octreotide group. Gallbladder bile total calcium (p < 0.05), bilirubin monoglucuronide (p < 0.05), total bilirubin (p < 0.01), total protein (p < 0.05), and total lipids (p < 0.05) were increased in the octreotide group. Animals receiving octreotide also had decreased hepatic (p < 0.05) and gallbladder (p < 0.001) bile pH. No differences in cholesterol saturation index were observed. These data suggest that in the prairie dog, octreotide (1) alters hepatic bile composition, (2) causes gallbladder stasis, and (3) increases gallbladder bile calcium, bilirubin, protein, lipid, and hydrogen ion concentrations. We conclude that octreotide causes alterations in gallbladder bile composition that increase the likelihood of cholesterol and calcium bilirubinate precipitation.
