Knoop M, McMahon R F, Braganza J M, Hutchinson I V
Department of Pathology, University of Manchester, England.
Am J Surg. 1989 Nov;158(5):452-8. doi: 10.1016/0002-9610(89)90285-7.
We describe our serendipitous finding of a transplantation model of hemorrhagic pancreatic necrosis. The slow evolution, from edematous interstitial pancreatitis to hemorrhagic necrosis over the course of 8 days made the model amenable to therapeutic manipulation. The possible pathogenesis is discussed with reference to the published literature. From comparisons between the histologic and biochemical features of isografts and allografts, we suggest that ischemia-reperfusion injury initiates pancreatitis through oxygen-free radicals, and that the transformation to hemorrhagic pancreatic necrosis in allografts reflects the involvement of chemotactic immune factors and extracellular secretions from activated proteases.
我们描述了我们偶然发现的出血性胰腺坏死移植模型。在8天的时间里，从水肿性间质性胰腺炎缓慢演变为出血性坏死，使得该模型适合进行治疗性操作。参考已发表的文献讨论了可能的发病机制。通过对同基因移植和异基因移植的组织学和生化特征进行比较，我们认为缺血再灌注损伤通过氧自由基引发胰腺炎，而异基因移植中向出血性胰腺坏死的转变反映了趋化免疫因子和活化蛋白酶的细胞外分泌的参与。
