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[急性胰腺炎的病因与发病机制]

[Etiology and pathogenesis of acute pancreatitis].

作者信息

Klar E

机构信息

Chirurgische Universitätsklinik Heidelberg.

出版信息

Helv Chir Acta. 1992 May;59(1):7-16.

PMID:1526849
Abstract

The pathogenesis of acute pancreatitis is based on the following principles: 1. Biliary. In biliary pancreatitis there is a causal relationship between the induction of acute pancreatitis and the migration of gallstones. The basic pathomechanism seems to be a combination of an increase in permeability and pressure in the ductal system. 2. Intraacinar. Caerulein-pancreatitis is a well established experimental model which reflects the intracellular/interstitial type of activation. Basolateral secretion of pancreatic enzymes into the interstitial space represents the initial event. Intracellular activation of trypsin by the fusion of zymogen-granules and lysosomes has been advocated as an alternative mechanism. 3. Alcohol. The acute alcohol pancreatitis comprises a combined pathogenesis. Obstruction and reflux as well as the cytotoxic effect of alcohol seem to be the main principles. 4. Disturbance of pancreatic microcirculation. Ischemia of the pancreas seems to play a key role in the transition from pancreatic edema to necrosis. Improvement of capillary perfusion by isovolemic hemodilution with dextran 60 has been shown to be an efficient therapeutic tool.

摘要

急性胰腺炎的发病机制基于以下原理

  1. 胆源性。在胆源性胰腺炎中,急性胰腺炎的诱发与胆结石的移动之间存在因果关系。基本病理机制似乎是导管系统通透性增加和压力升高的综合作用。2. 腺泡内。蛙皮素诱导的胰腺炎是一个公认的实验模型,反映了细胞内/间质型激活。胰腺酶从基底外侧分泌到间质空间是起始事件。有人提出,通过酶原颗粒与溶酶体融合导致胰蛋白酶在细胞内激活是另一种机制。3. 酒精性。急性酒精性胰腺炎具有复合发病机制。梗阻与反流以及酒精的细胞毒性作用似乎是主要原理。4. 胰腺微循环障碍。胰腺缺血似乎在胰腺水肿向坏死的转变中起关键作用。已证明用60右旋糖酐进行等容血液稀释以改善毛细血管灌注是一种有效的治疗手段。

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