The mechanism of cellular dysfunction after ischemia and reperfusion

本研究旨在阐明缺血再灌注引起的细胞功能障碍的机制和预防措施。结果表明：(1)心脏骤停7 min大鼠脑内脂过氧化物（LPO）升高，活动频率紊乱。心脏骤停前给予尼卡地平和尼莫地平对中枢神经系统抗缺氧有保护作用。(2)失血性休克、内毒素休克、内脏缺血休克等不同休克类型大鼠肝脏LPO浓度显著升高，黄嘌呤氧化酶（Xanthine oxidase， XOD）显著升高，超氧化物歧化酶（Superoxide dismutase， SOD）显著降低。(3)在一个将肺置于氧自由基生成系统中的模型中证实了细胞功能障碍。(4)用生物发光仪检测细胞中氧自由基的产生，荧光素作为光增强剂应用于组织匀浆上。(5)对内毒素休克大鼠和内脏缺血休克大鼠的脂质过氧化作用进行了评价。高剂量SOD可显著提高小鼠存活率。

the present study was undertaken to clarify the mechanism and to develop the preventive measures of cellular dysfunction induced by ischemia and reperfusion. The results are summarized as followed:(1)The rats with cardiac arrest for 7 min showed an incresed lipoperoxide (LPO) in the brain and disturbed ambulation frequency. Nicardipine and nimodipine given prior to the cardiac arrest showed a protective effect on the CNS against anoxia.(2)The rats with various types of shock such as hemorrhagic shock, endotoxin shock and splanchnic ischemia shock depicted significant elevations of hepatic LPO concentration, concomittantly with marked increases in Xanthine oxidase (XOD) and significant decreases in Superoxide dismutase (SOD).(3)The cellular dysfunction was certified in a model in which the lung was placed in an oxygen free radical production system.(4)The production of oxygen free radicals in the cells was detected by a bioluminescence machine using a lusiferine as a photo-intensifier applied on a tissue homogenates.(5)The effectiveness of various measures to prevent lipoperoxidation were evaluated in rats with endotoxin shock or splanchnic ischemia shock. A high dose of SOD elevated the survival rate significantly.