Altered sphincter of oddi phasic activity following truncal vagotomy

Neural as well as hormonal influences regulate sphincter of Oddi function. Therefore, we tested the hypothesis that truncal vagotomy alters sphincter of Oddi phasic activity and response to hormonal stimulation. Adult, male prairie dogs underwent either sham laparotomy or truncal vagotomy and pyloroplasty. Postoperatively, all animals were fed a trace-cholesterol (nonlithogenic) diet for 3 months. In acute terminal experiments the distal common bile duct was perfused with lactated Ringer's solution at 0.1 ml/min. Sphincter of Oddi (SO) phasic contractions as well as baseline resistance were recorded before and during a 30-minute intravenous infusion of 10 ng/kg/min of cholecystokinin-octapeptide (CCK-OP). Before the CCK-OP infusion, both the frequency and amplitude of SO phasic contractions were significantly greater (P < 0.01) in vagotomized animals. During CCK-OP, the frequency of SO phasic contractions remained significantly greater ( P < 0.01) in the vagotomy animals. The amplitude of SO phasic contractions, however, increased significantly (P < 0.03) in response to CCK-OP only in sham animals. Vagotomized animals failed to develop any further increase in the amplitude of SO phasic contractions during CCK-OP infusion. No differences in baseline resistance were noticed between sham and vagotomized animals before or during the infusion of CCK-OP. These findings suggest that (1) vagal tone inhibits sphincter of Oddi phasic contractions, (2) vagotomy increases sphincter of Oddi phasic activity, and (3) parasympathetic denervation alters the sphincter of Oddi's response to CCK-OP. Since the sphincter of Oddi plays an important role in normal gallbladder filling and emptying, altered sphincter of Oddi function may, in part, be responsible for the gallbladder stasis observed following vagotomy.