Antral control of gallbladder cyclic motor activity in the fasting state

The hypothesis that gastric antrum controls the phasic contractions of gallbladder cyclic motor activity in the fasting state was tested. Gallbladder, gastric, and small bowel motor and myoelectric activity was recorded by strain gauge transducers and bipolar electrodes. Gallbladder pressure was measured manometrically by a surgically implanted intraluminal catheter. After control recordings for 4 to 6 weeks, antrectomy and gastroduodenostomy were performed. Six weeks later, bilateral truncal vagotomy was performed in each dog. Recordings were made after each surgical procedure. In the control state, the gallbladder exhibited cyclic motor activity consisting of phasic contractions at a frequency of 0.75 ± 0.02/min superimposed on an increase in baseline pressure. Antrectomy and gastroduodenostomy completely abolished the phasic contractions of gallbladder cyclic motor activity and significantly decreased the incidence of the cyclic increase in baseline pressure. Subsequent vagotomy had no additional effect on gallbladder cyclic motor activity. In intact dogs, the gallbladder filled from 0% to 80% and emptied from 80% to 100% of the duodenal migrating motor complex cycle, which was considered to begin at the start of phase I activity. Antrectomy significantly altered this pattern; after antrectomy, the gallbladder filled from 0% to 10% and from 90% to 100% and emptied during the remainder of the duodenal migrating motor complex cycle. Subsequent vagotomy had no additional effect on periodic gallbladder filling and emptying. It is concluded that major changes occur in gallbladder cyclic motor activity and its periodic filling and emptying pattern in the fasting state after antrectomy and vagotomy. It is hypothesized that in the absence of cyclic phasic contractions after antrectomy, periodic stirring and agitation of gallbladder bile and its mixing with fresh hepatic bile may not occur in the fasting state. The absence of this phenomenon may lead to supersaturation of bile near the mucosal surface and increase the propensity for precipitation of salts and formation of gallstones.