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 divvided into 4 groups(n =8). Group I: The communicating branch between the dorsal and ventral pancreatic ducts was partly ligated Group IIa: The communicating branch was amputated and completely ligated Group IIb: 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 ductograhpy and the pathologic examination were made.RESULYS:The activities of serum PLA2 and ams in Group I,II a, and IIb were sigificantly increased 5-80 days after operation. At sacrifice, the basal pressures of the ventral duct were significantly wiaher 30min-60min after provocation in Group I, IIa and IIb. The pressures of the dorsal duct were significantly increased in Group IIb but no difference in Group I and IIa. Under light microscopy the fibrosis of interlobus and periducts, the destruction of acini and infiltratiob of inflammatory cell in dorsal and ventral pancreas were found in Group IIb. But in Group I and IIa, this findings were pesent only in ventral pancreas. The electron microscopy showed that in ventral pancreas of Group I and IIa and the dorsal and ventral pancreas of Group IIb, 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 oue of etiologic factors in chronic pancreatitis. The pathogenesis is the functional obstruction of the minor papilla at the peak stage of secretion.
AIM:To investigate the etiologic association of pancreas divisum (PD) with chronic pancreatitis and to clarify its pathogenesis. METHODS: A PDcanine model was established in 32 dogs. The dogs were randomly divvided into 4 groups(n =8). Group I: The communicating branch between the dorsal and ventral pancreatic ducts was partly ligated Group IIa: The communicating branch was amputated and completely ligated Group IIb: 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 ductograhpy and the pathologic examination were made.RESULYS:The activities of serum PLA2 and ams in Group I,II a, and IIb were sigificantly increased 5-80 days after operation. At sacrifice, the basal pressures of the ventral duct were significantly wiaher 30min-60min after provocation in Group I, IIa and IIb. The pressures of the dorsal duct were significantly increased in Group IIb but no difference in Group I and IIa. Under light microscopy the fibrosis of interlobus and periducts, the destruction of acini and infiltratiob of inflammatory cell in dorsal and ventral pancreas were found in Group IIb. But in Group I and IIa, this findings were pesent only in ventral pancreas. The electron microscopy showed that in ventral pancreas of Group I and IIa and the dorsal and ventral pancreas of Group IIb, 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 oue of etiologic factors in chronic pancreatitis. The pathogenesis is the functional obstruction of the minor papilla at the peak stage of secretion.