Abstract

Colonic motility was measured in normal human subjects after either a 350-calorie or a 1000-calorie meal and during the continuous infusion of gastrin I, octapeptide of cholecystokinin, or the 10% pure whole molecule of cholecystokinin. A bipolar clip electrode was used to record myoelectrical activity, and a perfused catheter was used to record intraluminal pressure. The percentage of total recording time during which slow wave activity was present and the slow wave frequency were not altered by either the meal or the gastrointestinal hormones. A 1000-calorie meal significantly increased spike and motor activity, but a 350-calorie meal minimally stimulated colonic motility. Serum gastrin increased during the 1000-calorie meal, but the time course of the maximum gastrin increase did not correspond to the peak colonic motility response. Spike and motor activity were significantly increased by gastrin I infused at a rate that maintained serum gastrin at levels present after a meal. Colonic motility was increased after the infusion of the octapeptide of cholecystokinin, but not after infusion of the 10% pure whole molecule of cholecystokinin. These studies suggest: (1) eating increases colonic motility with a greater effect occurring after the higher calorie meal; (2) gastrin I or the octapeptide of cholecystokinin can increase colonic motility at lower infusion rates than are necessary to produce their primary physiological effects; and (3) gastrointestinal hormones may mediate, in part, the response seen after eating, but may not be the sole factors.

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