粒细胞性胰腺炎的胰腺外器官损害。

Annales chirurgiae et gynaecologiae Pub Date : 1999-01-01
Z J He, M P Matikainen, H Alho, A Harmoinen, T Ahola, I Nordback
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引用次数: 0

摘要

背景与目的:多器官功能衰竭是急性胰腺炎的主要致命并发症。本实验研究1)急性胰腺炎模型胰腺外脏器损害的表现和时间过程,2)该模型中梗阻性肝损害是否因胰腺水肿压迫胆胰总管阻塞所致。材料与方法:80只雄性Wistar大鼠分为对照组和毛蛋白组(每组5个亚组)。小粒蛋白组腹腔注射小粒蛋白诱导急性胰腺炎。对照组注射等量生理盐水。两个亚组,一个是紫蛋白组,另一个是对照组,在注射前经十二指肠置入胰内胆管支架。非支架动物末次注射后1、6、12、24小时,支架动物末次注射后6小时,取胰腺、肝、肺、肾组织和血液标本,测定或分析间质水肿、血浆淀粉酶、丙氨酸转氨酶、胆红素、尿素、肌酐、碱性磷酸酶、乳酸脱氢酶、血气和电镜。结果:肺和肾没有变化。肝损害发生在最初的6-12小时,表现为血浆丙氨酸转氨酶和胆红素升高,电镜下胆管扩张和肝细胞损伤。胰内胆管支架不能解决这些变化。结论:在轻度水肿性胰腺炎模型中,肝脏可能是早期最先进化的胰外器官,肝细胞损伤不是由水肿性胰腺压迫胆总管阻塞引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Extrapancreatic organ impairment in caerulein induced pancreatitis.

Background and aims: Multiorgan function failures are the major fatal complications in acute pancreatitis. In this experiment, we studied 1) the manifestation and time course of extrapancreatic organ damage in an acute pancreatitis model and 2) whether the obstructive liver damage in this model is caused by the obstruction of common biliopancreatic duct compressed by oedematous pancreas.

Material and methods: 80 male Wistar rats were divided into two groups: control and caerulein groups (five subgroups in each group). In the caerulein group, the acute pancreatitis was induced by caerulein intraperitoneal injections. In the controls equal volume of saline was injected. Two subgroups, one in caerulein and one in control groups, had an intrapancreatic bile duct stent inserted transduodenally before the injections. The pancreas, liver, lung and kidney tissues and blood samples were obtained for the measurement or analysis of interstitial oedema, plasma amylase, alanine aminotransferase, bilirubin, urea, creatinine, alkaline phosphatase, lactate dehydrogenase, blood gas and electron microscopy at 1, 6, 12 and 24 hours after the last injection in unstented animals, and at 6 hours in stented animals.

Results: Lungs and kidney remained unchanged. Liver damage was found during the first 6-12 hours, manifest as increased plasma alanine aminotransferase and bilirubin and dilatation of bile canaliculi and hepatocyte damage in electron microscopy. The intrapancreatic bile duct stent did not resolve these changes.

Conclusions: The liver may be the first evolved extrapancreatic organ in the early stage in this mild oedematous pancreatitis model and the hepatocyte damage is not caused by the obstruction of common biliopancreatic duct compressed by the oedematous pancreas.

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