Abstracts
Copyright ©The Author(s) 1998. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 15, 1998; 4(Suppl2): 55-55
Published online Oct 15, 1998. doi: 10.3748/wjg.v4.iSuppl2.55
Experimental study on the etiologic effect of pancreas divisum on chronic pancreatitis and the pathogenesis
Hui He, Wei-Fang Lu, Yi-Min Zhang
Hui He, Wei-Fang Lu, Yi-Min Zhang, Department of Special Diagnosis, Chinese PLA 254 Hospital, Tianjin 300142, China
Author contributions: All authors contributed equally to the work.
Supported by National Natural Science Foundation of China, No.39370225.
Correspondence to: Dr. Hui He, Department of Special Diagnosis, Chinese PLA 254 Hospital, Tianjin 300142, China
Received: July 14, 1998
Revised: August 21, 1998
Accepted: September 11, 1998
Published online: October 15, 1998
Abstract

AIM: To investigate the etiologic association of pancreas divisum (PD) with chronic pancreatitis and to clarify the 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 remaining about 1.0 mm diameter. 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 am putation 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 performed.

RESULTS: (1) The activities of serum PLA2 and Ams in Group I,IIa and IIb were significantly increased 5 d-80 d after operation. (2) At sacrifice, the basal pressures of the ventral duct were significantly increased 30 min-60 min after provocation in Group I, IIa and IIb, especially in Group IIb, the pressures returned to the normal level till 90 min. The pressures of the dorsal duct were significantly increased in Group IIb but no difference in Group I and IIa. (3) Light microscope observation: The fibrosis of interlobus and periductes, the destruction of acini and infiltration of inflammatory cell in dorsal and ventral pancreas were found in Group IIb. But in Group I and IIa, these findings were present only in ventral pancreas. (4) Electron microscope observation: 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 relation. The zymogen granules decreased and the mitochondria was swollen.

CONCLUSION: A definite etiologic relationship was confirmed between PD and chronic pancreatitis. The pathogenesis was due to the functional obstruction of the minor papilla at the peak stage of secretion.

Keywords: Pancreas divisum/complications, Pancreatitis/etiology, Pancreatitis/physiopathology, Disease models, animal, Chronic diseases