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短暂性缺血对大鼠急性胰腺炎的发展及组织学模式的影响。

Effect of temporary ischemia upon development and histological patterns of acute pancreatitis in the rat.

作者信息

Spormann H, Sokolowski A, Letko G

机构信息

Institute of Pathological Anatomy, Medical Academy of Magdeburg, G.D.R.

出版信息

Pathol Res Pract. 1989 May;184(5):507-13. doi: 10.1016/S0344-0338(89)80143-8.

Abstract

To study the importance of a disturbed energy metabolism for the development of acute pancreatitis (AP) rats pretreated either by induction of a juice edema or by intraductal trypsin instillation were subjected to temporary pancreatic ischemia. By means of a scoring system quality and quantity of pathomorphologic parameters were quantified 24 h postoperatively. There was a clear correlation between macroscopic and histologic scores independent of the model used. While a juice edema or 40 min ischemia alone did not induce AP, a combination of both led in half of the animals treated to AP. This was mainly characterized by extrapancreatic fat necrosis. Besides less specific fat necrosis the histologic examination of the pancreas revealed acinar necroses at the periphery of the lobules as a frequent injury pattern. After trypsin injection a persistent pancreatic edema, hemorrhages, fat and parenchymal necroses were typical findings. Both focal centro-lobular and extended sublobular or lobular necroses were histologically observed. An additional temporary ischemia augmented significantly the severity of findings, however, their quality was not essentially changed. From the present results it can be concluded that an alteration of the pancreatic energy metabolism, e.g. by hypoperfusion or ischemia, may be an important pathogenic factor in precipitating experimental AP.

摘要

为研究能量代谢紊乱在急性胰腺炎(AP)发病中的重要性,对预先通过诱发胰液性水肿或经导管注入胰蛋白酶处理的大鼠进行短暂性胰腺缺血。通过评分系统对术后24小时病理形态学参数的质量和数量进行量化。无论使用何种模型,宏观评分与组织学评分之间均存在明显相关性。单独的胰液性水肿或40分钟缺血不会诱发AP,但两者结合会导致半数接受治疗的动物发生AP。这主要表现为胰腺外脂肪坏死。除了不太特异的脂肪坏死外,胰腺组织学检查显示小叶周边的腺泡坏死是常见的损伤模式。注射胰蛋白酶后,持续性胰腺水肿、出血、脂肪和实质坏死是典型表现。组织学观察到局灶性小叶中心坏死以及扩展性小叶下或小叶坏死。额外的短暂性缺血显著加重了病变的严重程度,但其性质并未发生本质改变。从目前的结果可以得出结论,胰腺能量代谢的改变,如通过低灌注或缺血,可能是诱发实验性AP的一个重要致病因素。

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