Original Articles
Copyright ©The Author(s) 1998. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 1998; 4(6): 533-535
Published online Dec 15, 1998. doi: 10.3748/wjg.v4.i6.533
An experimental study in etiologic effect of pancreas divisum on chronic pancreatitis and its pathogenesis
Hui He, Wei-Fu Lu, Ya-Zhu Ke, Yi-Min Zhang
Hui He, Wei-Fu Lu, Ya-Zhu Ke, Yi-Min Zhang, Department of Special Diagnosis, Chinese PLA 254 Hospital, Tianjin 300142, China
Hui He, born on 1971-12-12 in Tianjin, graduated from Tianjin Medical University in 1995, having 3 papers published.
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Hui He, Department of Special Diagnosis, Chinese PLA 254 Hopital, 160 Wu Ma Lu, Tianjin 300142, China
Telephone: +86-22-26355985
Received: June 10, 1998
Revised: August 20, 1998
Accepted: November 10, 1998
Published online: December 15, 1998

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 2 mm 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.

RESULTS: The activities of serum PLA2 and ams in Group I, IIa, and IIb were sigificantly increased 5-80 d after operation. At sacrifice, the basal pressures of the ventral duct were significantly wiaher 30 min-60 min 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 one of etiologic factors in chronic pancreatitis. The pathogenesis is the functional obstruction of the minor papilla at the peak stage of secretion.

Keywords: pancreatitis/etiology, pancreatitis/physiopathology, paucreas divism/physiopathology, paucreas divism/etiology, chronic diseases