AIM To investigate the etiologic association of pancreas divisum (PD) with chronic pancreatitis and to clarify its pathogenesis. METHODS A PD canine model was established in 32 dogs. The dogs were randomly divided into 4 groups (n = 8). Group I : The communicating branch between the dorsal and ventral pancreatic ducts was partly ligated. Group II a: The communicating branch was amputated and completely ligated. Group II b: The dorsal duct was amputated and ligated at 2mm distance to the minor papilla. Group III: A sham operation without any amputation or ligation was performed. Before and after operation, the activities of serum phospholipase A2 (PLA2) and amylase (Ams) were assayed and the basal pressures of the ducts were measured when secretin was injected. Pancreatic ductography and the pathologic examination were made. RESULTS The activities of serum PLA2 and Ams in Group I, II a and II b were significantly increased 5 - 80 days after operation. At sacrifice, the basal pressures of the ventral duct were significantly higher 30min - 60min after provocation in Group I, II a and II b. The pressures of the dorsal duct were significantly increased in Group II b but no difference in Group I and II a. Under light microscopy the fibrosis of interlobus and periducts, the destruction of acini and infiltration of inflammatory cell in dorsal and ventral pancreas were found in Group II b. But in Group I and II a, these findings were present only in ventral pancreas. The electron microscopy showed that in ventral pancreas of Groups I and II a and the dorsal and ventral pancreas of Group II b, the rough endoplasmic reticulum of the acinar cells showed granules-scaling, fusion and dilatation. The zymogen granules decreased and the mitochondria was swollen. CONCLUSION PD is one of etiologic factors in chronic pancreatitis. The pathogenesis is the functional obstruction of the minor papilla at the peak stage of secretion.