The aim of this study was to elucidate the importance of biliary output for the regulation of migrating motor complex and the release of plasma motilin. Gallbladder emptying was monitored by hepatobiliary scintigraphy, plasma motilin concentration by radioimmunoassay and gastrointestinal motility by a perfused catheter system. During a total recording time of 46 h and 20 min in 16 volunteers, we observed 29 episodes of gallbladder emptying, 27 plasma motilin peaks and 23 activity fronts (phase 3 activity) of the migrating motor complex (MMC). Twelve episodes of gallbladder emptying started in phase 1 and continued into phase 2 of the MMC. The remaining 17 episodes of gallbladder emptying started in phase 2, and three of these continued into phase 3 of the MMC. Biliary output was associated with a significant rise in plasma motilin concentration, whereas plasma motilin significantly decreased after the activity fronts. These observations may explain the well-known fluctuations of plasma motilin concentration in the fasted state. Motilin is released into the circulation as a result of biliary output, while the ensuing activity front of the MMC removes this stimulant from the proximal small bowel, resulting in a fall in plasma motilin. In conclusion, we have confirmed a temporal relationship between biliary output into the duodenum and the release of plasma motilin. The observed transition from phase 1 to phase 2 and from phase 2 to phase 3 of the MMC during gallbladder emptying episodes suggests that biliary output stimulates gastrointestinal motility in the fasted state.
Interdigestive motility of the small intestine was examined in 23 fasted healthy volunteers following luminal administration of the prostaglandins E2 and F2 alpha. Motility was monitored by means of water-perfused catheters measuring intraluminal pressure changes. The registration points were located 25 cm apart, in the proximal duodenum, at the angle of Treitz, and in the jejunum. Prostaglandin E2 administered intraduodenally delayed the initiation of the subsequent activity front. The interval to the next activity front was prolonged by a dose of 1.0 mg prostaglandin E2 from 79.5 +/- 9.5 min to 137.1 +/- 5.0 min (P less than 0.01) and to 158.0 +/- 14.0 min by 2.0 mg prostaglandin E2 (P less than 0.05). Also, in four of seven experiments, a progressing activity front was arrested by 2.0 mg prostaglandin E2. Prostaglandin F2 alpha at 2.5 or 5.0 mg given intraduodenally induced bursts of contractions with a frequency of 17.7 +/- 0.8 contractions per minute and an amplitude of 10 to 110 mm Hg (P less than 0.01). In comparison, food intake produced irregular contractions at a frequency of 5.3 +/- 1.8 contractions per minute and an amplitude of 10 to 50 mm Hg (P less than 0.05). It is concluded that prostaglandin E2 delays the initiation of activity fronts in the duodenum. In contrast, prostaglandin F2 alpha changes the interdigestive motility pattern to one of intense contractile activity, which is different from the postprandial motility pattern.
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