Abstract
The role of cholecystokinin (CCK) in postprandial control of colonic motility is controversial. To test the hypothesis that CCK stimulates colonic tone, motility, and transit we measured these colonic functions in 16 healthy subjects using intraluminal manometry, barostatic balloon measurements, and radioscintigraphy. This was a randomized-order, double-blind, sequential study design in each subject of saline and either atropine (0.01 mg/kg stat and 0.01 mg/kg/hr by infusion) or CCK-octapeptide (OP, 30 ng/kg stat and 60 ng/kg/hr by infusion). Atropine was used as control to demonstrate responsiveness of selected parameters of colonic motility. Atropine significantly reduced whole colon (change from fasting = 52 +/- 11%) and left colon (change from fasting 61 +/- 8%) phasic pressure activity and transverse colon tone (change from fasting 159 +/- 40%); CCK-OP had no significant effects on phasic contractility, tone or transit. Thus, a CCK-OP infusion that maximally stimulates pancreatic exocrine secretion and gallbladder contraction has no effect on motor function or transit in prepared colon of healthy subjects.
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