Gallbladder volume and interdigestive gastric and duodenal motor activity were evaluated simultaneously in 12 normal subjects. After overnight fasting, gallbladder volume was monitored every 4 min in each subject by means of real-time ultrasonography, and gastroduodenal motor activity was measured by means of a probe consisting of three polyvinyl catheters with one side opening for each catheter, placed 15 cm apart and constantly perfused with deionized water. Real-time ultrasonography and intestinal manometry were performed by different investigators and continued until at least two consecutive spontaneous phase III activities of migrating motor complexes were observed. The results show a cyclic variation of gallbladder volume, which reached its minimum value before the end of phase II in the proximal duodenum and its maximum in early phase II, 25 min after the beginning of phase III. These results suggest that there is a relationship between the cyclic gallbladder volume changes, which occur during fasting in humans, and with the various phases of duodenal migrating motor complex.

The effect of direct cholinergic stimulation and blockade on gallbladder volume, determined by real-time ultrasonography (RUS), was evaluated in twenty normal, fasting subjects. Eleven subjects received atropine sulphate or placebo and 9 subjects a series of 3 injection of prostigmine, bethanechol or placebo, randomly assigned, at intervals of 24 h. RUS was performed under basal conditions after fasting for 12 h and every 5 min after drug injection up to 45 min in the atropine study and up to 60 min after prostigmine and bethanechol. There was no significant variation from fasting gallbladder volume after placebo in either group. After atropine sulphate gallbladder volume at first decreased and then significantly increased. With bethanechol and prostigmine, the volume fell significantly to a trough after 30 to 35 min, and then it returned to the basal value within 60 min. It is suggested that cholinergic mediation is involved in maintaining fasting tone in the gallbladder and that cholinergic stimulation causes contraction of the gallbladder by a direct effect.

To evaluate the influence of the stomach and the cholinergic system on gallbladder contraction induced by physiological stimuli, the reduction in gallbladder volume in 7 healthy volunteers has been studied by real-time ultrasonography after the oral and intraduodenal administration of olive oil, preceded by pretreatment with cimetropium bromide or placebo. After an overnight fast, each subject swallowed 50 ml olive oil or it was administered through a naso-duodenal tube in the proximal duodenum. Cimetropium bromide 5 mg or placebo was given intravenously under double-blind control. After the placebo pretreatment, gallbladder contraction was greater and faster after intraduodenal oil than after oral oil. Cimetropium bromide decreased the extent, velocity and duration of gallbladder contraction induced by intraduodenal olive oil but it only reduced the velocity of the contraction induced by oil given orally. It is concluded that in normal human subjects the stomach modulates the extent and velocity of postprandial gallbladder contraction and that anticholinergic agents antagonize the gastric and duodenal phases of the response of the gallbladder to a meal.

We examined the refractory period of the migrating motor complex and the ability of somatostatin to increase the oscillation frequency of the complex through the initiation of premature phase HI activity. Fifteen normal human subjects were studied by means of a naso‐intestinal motility probe and divided in three groups of five subjects each. After recording three spontaneous migrating motor complexes, somatostatin was infused at a time interval from the last spontaneous Phase III that corresponded to 10% (Group A), 20% (Group B) and 30% (Group C) of the previous mean cycle length. Eleven successive somatostatin infusions were given with the interval between each infusion being altered in a fashion designed to identify the refractory period of the MMC. The results show a spontaneous cycle length of 121.3 ± 15.8 min (mean ± SD). When given at 10% (12 min) of the previous cycle somatostatin did not elicit any response, when given at 20% (24 min) of the cycle somatostatin induced a premature Phase III activity in three of five subjects; when given at 30% (36 min) of the cycle somatostatin induced a premature Phase III in all five subjects examined. Each somatostatin infusion was associated with the onset of a premature Phase III activity in 50% of the trials when the time interval was 20% of the ideal cycle (24 ± 4 min). When the time interval was increased to 30% of the ideal cycle a premature Phase III could be recorded after each somatostatin infusion in all trials. Motilin and pancreatic polypeptide plasma levels were significantly lowered by somatostatin. It is concluded that the migrating motor complex of the human gastrointestinal tract shows an absolute and a relative refractory state. Repetitive infusions of somatostatin for short periods may increase the occurrence of Phase III activity up to four‐fold.

There is an increased incidence of gallstones in patients who have undergone Billroth II (BII) gastrectomy for duodenal ulcer. To explore the mechanisms underlying this, we examined changes in gallbladder volume induced by a meal and by intravenous administration of cerulein, in 13 BII patients and in 13 normal subjects. Gallbladder volume was measured by real-time ultrasonography. In the fasting state, gallbladder volumes were significantly larger in BII patients than in controls. The percent decrease in gallbladder volume after the meal was significantly less and maximum volume reduction observed throughout the study occurred sooner in BII patients than in controls. In contrast, the kinetics and magnitude of the reduction in gallbladder volume induced by cerulein were similar in the two groups. These findings suggest that the altered gallbladder response to a meal is due to impaired postprandial stimulation of gallbladder following BII gastrojejunostomy.