The mechanism of cellular dysfunction after ischemia and reperfusion

本研究旨在阐明缺血再灌注所致细胞功能障碍的机制，并探讨其预防措施。结果如下：(1)大鼠心脏骤停7min后，脑组织过氧化脂质(LPO)含量升高，活动频率紊乱。在心脏骤停前给予尼卡地平和尼莫地平对中枢神经系统有保护作用。(2)失血性休克、内毒素休克和内脏缺血休克等不同类型休克大鼠肝脏LPO含量显著升高。(3)在将肺置于氧自由基产生系统的模型中，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。(5)对内毒素休克和内脏缺血休克大鼠进行了各种防止脂质过氧化的措施的有效性评价。高剂量的超氧化物歧化酶可显著提高小鼠的存活率。

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.