Shneĭvas V B, Amilov K S, Levin G S
Patol Fiziol Eksp Ter. 1994 Jan-Mar(1):27-30.
The authors examined the contribution of lipid peroxidation (LPO) in the pathogenesis of hepatic damage in visceral and ischemic shock (VIS) induced by upper mesenteric artery occlusion followed by stepwise revascularization. There was generation of initial and terminal PLO products in hepatic tissue, which increased as VIS and toxemia progressed. The accumulation kinetics of thiobarbituric acid-positive agents in the hepatic homogenates, microsomes, and mitochondria isolated in different periods of VIS was studied. The findings confirm the hypothesis that oxygen radicals play a role in the development of disturbances typical of those in the liver during the shock.
作者研究了脂质过氧化(LPO)在肠系膜上动脉闭塞继以逐步血管再通所诱发的内脏和缺血性休克(VIS)肝损伤发病机制中的作用。肝组织中出现了初期和终末期PLO产物,且随着VIS和毒血症的进展而增加。研究了在VIS不同时期分离出的肝匀浆、微粒体和线粒体中硫代巴比妥酸阳性物质的蓄积动力学。这些发现证实了以下假说,即氧自由基在休克期间肝脏典型紊乱的发展中起作用。