A brief report is given on the possible role of oxygen-derived free radicals and cholecystokinin in the pathogenesis of experimentally induced acute pancreatitis. Furthermore, use of scavengers (superoxide dismutase, catalase), CCK-receptor antagonists and somatostatin are discussed in the therapy of acute pancreatitis induced in animal models. It is suggested that both the term of direct pancreatic cytoprotection of the above-mentioned agents and the validity of the animal models used for induction of acute pancreatitis have to be reconsidered.