胰腺分裂与慢性胰腺炎的病因学关系及发病机制

An experimental study on the etiologic effect of pancreas divisum on chronic pancreatitisand the pathogenesis

目的:探讨胰腺分裂(PD)在慢性胰腺炎病因学中的作用及其发病机制。方法:将32只犬随机分为4组(每组8只)。Ⅰ组:部分结扎背-腹胰管间的交通支。Ⅱa组:切断并结扎交通支。Ⅱb组:在背胰管注入小乳头前2mm处将其切断并结扎断端。Ⅲ组:假手术对照组,除不结扎交通支外,其余操作同上。于手术前检测各组犬血清磷脂酶(PLA2)和淀粉酶(Ams)活性及背、腹胰管基础压并在胰泌素激发后15、30、45、60和90分钟各测压一次。于术后180天再行胰胆管测压和造影并观察背、腹胰和十二指肠乳头的病理改变。结果:⑴Ⅰ、Ⅱa组和Ⅱb组术后5-80天血清PLA2和Ams活性显著升高。⑵处死时Ⅰ、Ⅱa组腹胰管和Ⅱb组背、腹胰管压力在激发后30-60分钟显著高于注药前(P<0.01);在60分钟后,前两组压力恢复到术前水平(P>0.05),而Ⅱb组仍较高(P<0.05),该组压力在90分钟后恢复正常。⑶光镜:Ⅱb组犬背、腹胰小叶间或/和胰管周围显著纤维组织增生,腺细胞结构破坏和炎细胞浸润。Ⅰ和Ⅱa组腹胰见轻度上述改变。⑷电镜:Ⅰ、Ⅱa组腹胰和Ⅱb组背、腹胰腺细胞粗面内质网脱颗粒、融合和扩张。酶原颗粒减少,线粒体肿张。Ⅰ和Ⅱa组背胰及Ⅲ组背、腹胰未见异常。结论:PD是慢性胰腺炎的病因学因素之一,其引发胰腺炎的机制是在胰液分泌的高峰期副乳头功能性梗阻。?

Objective To clarify the etiologic associatio n of pancreas divisum(PD)with chronic pancreatitis and the pathogenesis.Methods Acanine model of PDwas established i n 32dogs.The dogs were randomly divided into 4groups(n =8).Group I:The communicating branch b etween the dorsal and ventral pancre atic duct was partly ligated re-mainding a 1.0mmdiameter.GroupⅡa:The communicating branch was amputated and competely ligated.GroupⅡb:The dorsal duct was amputated and lig ated at 2mm distance to the minor papi lla.GroupⅢ:A sham operation without any amputation or ligation was perfo rmed.Before and after operation,th e activities of serum phospholipase A2(PLA2)and amylase(Ams )were assayed and the basal pressures of the ducts were measured when secre tin was in-jected.Pancreatic ductography and the pathologic examination were performed.Results(1)The activities of serum PLA2and Ams in GroupⅠ,Ⅱa andⅡb were significantly increased 5-80days after operation.(2)At sacrifice,the especially in Group Iand IIa.(3) Light microscope: the fibsis of intrelobus and peri-ducts, the destruction of acini and infiltration.(4) Electron microscope; In ventral pancreas of Group I and IIa and the dorsal .The pathogenesis was due to the functional obstruction of the minor papilla at the peak stage of secretion.