摘要
目的探讨肝脏缺血再灌注(I/R)损伤的发生机制,观察乌司他汀(UTI)对肝脏I/R损伤的保护作用。方法选择外伤性肝破裂手术中行肝门阻断术患者38例,随机分为I/R组和UTI组各19例。观察肝脏I/R后血清TNF、MDA、AST、ALT变化及再灌注肝组织多形核白细胞(PMN)浸润和肝组织形态学变化。结果I/R组:血清TNF、MDA、AST、ALT显著升高,肝组织PMN浸润明显增加。电镜下可见肝窦内皮细胞破坏,肝细胞线粒体结构改变。UTI组:血清TNF、MDA、AST、ALT明显降低。肝组织PMN浸润明显减少,肝组织超微结构明显改善。结论肝脏I/R诱导TNF产生。UTI能明显减轻PMN依赖性肝脏I/R损伤。
Objective To investigate the pathogenesis of hepatic ischemic-reperfusion (I/R) injury and observe the protection of ulinastatin on the liver. Methods Thirty-eight patients with hepatorrhexis undertaken hepatic hilum occlusion were selected. All patients were randomly divided into I/R group and ulinastatin group. Serum levels of tumor necrosis factor (TNF),malondialdehyde (MDA),aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were tested. The hepatic morphological changes were observed and the number of infiltrated neutrophil in liver tissue at 60 minutes of reperfusion was counted. Results Serum levels of TNF,MDA,AST and ALT in the I/R group were significantly higher than those in the ulinastatin group. Under light microscopy, neutrophils infiltration of liver tissue increased significantly, and electronic microscopic revealed that the hepatic sinusoidal endothelial cells and the hepatocellular mitochondria were injured in the I/R group. Pre_treatment with ulinastatin was able to significantly improved the pathological changes and decreased the hepatic I/R injury. Conclusion Hepatic I/R induce to release TNF-α,liver tissue is protected effectively from I/R injury by the ulinastatin pre_treatment.
