肠缺血-再灌流损伤时自由基对肺损伤作用的探讨

The action of free radical on lung damage during intestinal ischemic-reperfusion injury

动态观测了家兔肠缺血—再灌流时入肺血和出肺血超氧化物歧化酶(CuZn-SOD)以及脂质过氧化代谢产物丙二醛(MDA)的含量。正常时出肺血SOD的含量高于入肺血,P<0.05;入肺血的MDA含量高于出肺血,P<0.05。再灌流初期入肺血SOD含量增加,而出肺血SOD变化不明显。后期入肺血SOD含量高于出肺血,P<0.05;肺组织的SOD含量比正常时的减少,P<0.05;入肺血及出肺血的MDA含量均明显升高。结果提示正常时肺组织的SOD活性较高对清除氧自由基有重要的生理意义;肠缺血—再灌流损伤初期肺对SOD相关的代谢具有一定的调整作用,后期自由基的增多可致肺组织的损伤。

The concentrations of CuZn-SOD and malondialdehyde (MDA) in in-flowingand out-going pulmonary blood(IPB, OPB) were observed dynamically during intestinal ischemic-reperfusion in rabbits. The results showed that in normal subjects the content of SOD of OPB was higher than IPB, P<0.05; MDA of IPB was higher than MDA of OPB, P<0.05. In the early stage of reperfusion SOD of IPB increased, but SOD of OPB showed no significant change, at the later stage SOD of IPB was higher than SOD of OPB, P<0.05; SOD of lung tissue decreased; MDA of IPB and OPB increased significantly. It is suggested that in normal the higher SOD activity of lung tissue has important physiologic significance for scavenging oxygen free radical, lung might regulate the metabolism of SOD during the initial period of intestinal ischemic-reperfusion injury, and increasing free radicals might induce the damage of lung tissue during the later period.