A role for the brain/gut peptide cholecystokinin (CCK) in the control of gastric emptying has been proposed. In the present studies, we have used a potent type A CCK-receptor antagonist (devazepide) to examine the quantitative contribution of endogenously released CCK in the control of liquid gastric emptying of 100 ml lipid, protein, and carbohydrate test loads in rhesus monkeys. Emptying was studied in conscious monkeys equipped with chronic indwelling gastric cannulas. Prior intragastric administration of devazepide (1.0-320 micrograms/kg) differentially affected the 10-min emptying of glucose (0.125/ml), peptone (4.5%), and Intralipid (4.5%). Glucose emptying was not affected by any dose of the CCK antagonist. The emptying of peptone was accelerated by doses of 10 micrograms/kg or higher. This effect, however, was only partial and plateaued at a dose of 100 micrograms/kg. The gastric emptying of Intralipid was accelerated at a dose of 32 micrograms/kg, and the inhibitory effect of the Intralipid was completely eliminated at a dose of 320 micrograms/kg. At this dose of devazepide, the Intralipid test meal emptied from the stomach at the same rate as physiological saline. These data demonstrate that in rhesus monkeys endogenously released CCK 1) does not play a role in the control of glucose emptying, 2) is a partial mediator of the inhibitory action of peptone on gastric emptying, and 3) is the primary inhibitory mediator in the control of the gastric emptying of Intralipid.
Classical Cesarean Section
