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急性胰腺炎发病机制中的实验与临床相关性

Experimental and clinical correlation in acute pancreatitis pathogenesis.

作者信息

Stoian M, Dragomir C, Dăscălescu C, Pădureanu S, Damian M

机构信息

Department of Surgery, Universitatea de Medicină şi Farmacie Gr. T. Popa, Iaşi.

出版信息

Rev Med Chir Soc Med Nat Iasi. 1995 Jan-Jun;99(1-2):82-9.

PMID:9524660
Abstract

Pathological aspects in 100 cases of operated A.P. different in severity are not strictly related to aetiological conditions. Clinical observations have suggested some components of pathogenesis: obstruction of bilio-pancreatic inflow in duodenum at the beginning of the attack, bilio-pancreatic reflux on cholangiograms, strong secretory digestive stimulation before attack. Some experimental animals models (dogs) which can mimic pathogenic mechanism (obstruction of pancreatic flow, common bilio-pancreatic duct, closed duodenal loop, acute cholecystitis) have revealed characteristic pathological changes depending on the initiating process. Our conclusion that severity of pathological changes in A.P. are determined by the initiating mechanisms which may differ in some aetiological condition or may be common for different ones.

摘要

100例不同严重程度的急性胰腺炎手术病例的病理表现与病因学情况并无严格关联。临床观察提示了发病机制的一些要素:发作开始时十二指肠内胆胰液流入受阻、胆管造影显示胆胰反流、发作前强烈的分泌性消化刺激。一些能够模拟致病机制(胰液流动受阻、胆胰共同管阻塞、十二指肠闭合环、急性胆囊炎)的实验动物模型(狗)已显示出取决于起始过程的特征性病理变化。我们的结论是,急性胰腺炎病理变化的严重程度由起始机制决定,这些起始机制在某些病因学情况下可能不同,或在不同病因中可能相同。

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