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Just as cyclic changes in motility and secretions occur during fasting, recent evidence demonstrates that duodenogastric reflux during fasting is also cyclic and related to the motility and secretory variations. We investigated the characteristics of the migrating motility complex and duodenogastric reflux in 17 patients with gastric ulcer and compared these characteristics to those of 16 healthy subjects. We found three abnormalities of the complex in patients with gastric ulcer: (1) the antral motility was significantly decreased during the phase II of the complex (P less than 0.05) when compared to controls; (2) in about two thirds of them, the phase III of the complex was initiated at the duodenum or more distally; and (3) the mean bile salt concentration in the gastric aspirate was significantly higher (P less than 0.05) than that of the controls. We observed no relationship between the ulcer activity, the location of the crater, and the motility or reflux abnormalities.

Pressure measurements of the whole extrahepatic biliary tract were performed in dogs using constant perfusion techniques. Studies were done during general anesthesia and in conscious trained dogs. Gallbladder intraluminal fasting pressure was significantly lower than common bile duct pressure. No motor activity was demonstrated in the common bile duct. At the cysticocholedochal junction a static high-pressure zone was observed, probably due to mechanical factors. At the level of the choledochoduodenal junction, a high-pressure zone with a sphincter behavior was demonstrated, with a resting pressure of 38 cm H2O above intraduodenal pressure and with rhythmic contractions with a mean amplitude of 88 cm H2O above duodenal pressure. Duodenal motility was completely different from sphincter dynamics. No differences in pressure values were seen during general anesthesia or in conscious state.

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The physiological role of gastrin in H+ secretion is well established. We decided to study the effects of physiological doses of gastrin (as evidenced by H+ secretion and postprandial serum gastrin levels) on antroduodenal motility in order to delineate its role in antral motility regulation. Nine healthy male subjects, mean age 31 years, had two studies on different days. On day 1, gastroduodenal motility was monitored with a continuously perfused catheter system while gastric secretions were aspirated. After a basal period of 45 min, human synthetic gastrin (hG-17) was infused intravenously in consecutive doses of 6.25, 25, 100, and 400 pmol/kg/hr during 45 min each. On day 2, all subjects had a standard protein meal. Blood was withdrawn on both days for gastrin measurement by RIA. Increasing amounts of hG-17 caused a stepwise increase in serum gastrin and acid output. The D50 for H+ secretion was 25 pmol/kg/hr hG-17. The mean postprandial gastrin level was 31 +/- 5 pM, a level which was comparable to that seen during infusion of hG-17 6.25 pmol/kg/hr. At these serum gastrin levels, antral motility was either reduced or unchanged. Duodenal motility was unchanged. A reduction in the antroduodenal motility ratio was seen at these levels, but there was no interruption of the interdigestive motility complex. These results suggest that at physiological levels, gastrin by itself does not seem to have a major role in human antroduodenal motility regulation.

No abstract