移植肝再灌注损伤的发生机制

目的：介绍有关移植肝再灌注损伤发生机制的研究动向，方法：复习有关文献并进行综述性报告。结果：移植肝冷保存后的再灌注损伤的发生机制主要有：（1）内皮细胞损伤和Kupffer细胞激活，导致一系列细胞因子的产生，引起移植肝损伤，并引发全身炎症反应综合征。（2）白细胞，血小板与肝血窦壁的粘附而损害肝细胞，并可阻塞肝血窦造成“无复流”现象；（3）pH值的变化，再灌注后移植肝的代谢恢复正常后，组织内pH值的改变可引起肝细胞损伤，并可造成线粒体的肿胀，使肝细胞的功能降低，（4）复氧损伤，主要与白细胞释放活性氧（ROS）有关，结论：移植肝再灌注损伤是多种因素综合作用的结果，在再灌注前后提高肝细胞和内皮细胞的活性，抑制Kupffer细胞的激活，减少ROS及肿瘤坏死因子（TNF）的产生将是今后预防移植肝再灌注损伤研究的关键。

Mechnisms of ischemia/reperfusion injury in transplanted liver

Objective　To introduce the research trence of the medchnisims of ischemia/reperfusion(I/R) injury in transplanted liver(TL). Methods　Making a literature summarization based on papers review.Results　The main mechnisms of I/R injury in TL as the followings: (1) Production of various cytokines resulted from endothelial cell injury with activation of kupffer cells, which can result in TL injury and induce systemic inflammation syndrom. (2) White blood cells and platelets adhere to the liver sinusoid (LS), which can cause TL injury and obstruct the LS causing “no reperfusion" of TL. (3) Alteration of pH in the cells of TL. After recovery of normal metabolism of the reperfused TL, alteration of pH in the TL can cause damage to TL cells, and cause edema of mitochrondria resulting in decresing of TL function. (4) Reoxygenation injury mainly caused by activated oxygen relsased by white blood cell. Conclusions　I/R injury of TL is caused by combination of muttiple foctors. Improving the activity of hepatocytes and endothelial cells, imhibiting the activation of kupffer cells, decreasing the production of activated oxygen and TNF are the key points in preventing I/R injury of TL.