To assess the role of endogenous cholecystokinin in the control of gastric
emptying of peptone solutions and Intralipid suspensions, we examined the a
bility of a dose range of the CCK-A antagonist, devazepide to accelerate th
e gastric emptying of various caloric concentrations of peptone and Intrali
pid in rats. In the absence of devazepide, both peptone and Intralipid empt
ying slowed with increasing concentration. Devazepide's effect on peptone g
astric emptying diminished with increasing peptone concentration. The thres
hold dose for accelerating the emptying of 0.2 kcal/ml peptone was lower th
an the threshold dose for affecting 0.5 kcal/ml peptone and devazepide had
no effect on the gastric emptying of 1.0 kcal/ml peptone. In contrast, deva
zepide affected Intralipid gastric emptying at all three Intralipid concent
rations and the threshold dose decreased with increasing Intralipid concent
ration. However, the magnitude of the effect of devazepide on peptone or In
tralipid gastric emptying was partial and did not increase as a function of
concentration. These data demonstrate a role for endogenous CCK in the emp
tying of peptone and Intralipid but suggest that endogenous CCK does not ac
count for the increased slowing of gastric emptying evident with increased
caloric concentration (C) 2000 Elsevier Science B.V. All rights reserved.