Portacaval shunt increases the trophic effect of cholecystokinin on the rat pancreas.

The trophic effect of cholecystokinin (CCK) on the pancreas was examined in portacava-shunted (PCS) rats. Exogenous CCK-8s and the CCK-A receptor antagonist devazepide were infused continuously by means of osmotic minipumps. HyperCCKemia of endogenous origin was induced by pancreaticobiliary diversion (PBD), which is known to cause growth of the pancreas. The results showed that PCS as such was without a trophic effect on the pancreas, whereas the combination of CCK-8s and PCS or PBD and PCS increased the trophic effects on the pancreas compared with CCK-8s or PBD alone. Moreover, the trophic effects of PBD and of the combination of PBD and PCS could be prevented by CCK-A receptor blockade (devazepide infusion). The results suggest that the capacity of the pancreas to respond to CCK is exaggerated--for as yet unknown reasons--after PCS.