Evidence based on animal studies suggests that cholecystokinin (CCK) is inv
olved in the induction and development of acute experimental pancreatitis.
However, the results obtained with CCK or CCKA receptor antagonists in diff
erent species (rats, mice) and different models of acute pancreatitis (ceru
lein pancreatitis, hemorrhagic pancreatitis induced by choline-deficient, e
thionine-supplemented diet, arginine-induced pancreatitis, sodium taurochol
ate-induced pancreatitis) produced variable results. The route of administr
ation, the specificity and potency of compounds and the design of the study
are predictive for the outcome. Based on the available information, CCK ap
pears to play a contributory role in the development of acute experimental
pancreatitis in mice and rats. No conclusions can be drawn from these resul
ts with respect to the human disease.