ω-3脂肪酸后处理对大鼠缺血再灌注心肌抗氧化作用的影响

Effect of omega-3 fatty acids postconditioning on antioxidation of rats myocardium during ischemia reperfusion injury

目的探讨ω-3脂肪酸后处理对离体大鼠缺血再灌注心肌抗氧化作用的影响。方法将60只SD大鼠随机分为4组:持续灌注组(A组)、缺血再灌注组(B组)、缺血后处理组(C组)以及ω-3脂肪酸后处理组(D组)。建立Langendorff离体大鼠心脏缺血再灌注模型,A组持续灌注150min,其余各组均平衡灌注30min,全心缺血30min,再灌注90min,C组在再灌注开始前进行4个循环的复灌20s/缺血20s,D组在再灌注开始前用ω-3脂肪酸灌注15min。灌流结束后取左心室心肌测定超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)水平;透射电镜下观察心肌线粒体形态结构的改变,TTC染色计算心肌梗死面积。结果与B组相比,C、D组LDH、MDA水平显著降低(P<0.05),D组SOD水平显著升高(P<0.05);C、D组的大鼠心肌线粒体损伤程度明显减轻,心肌梗死面积明显缩小(P<0.01)。结论ω-3脂肪酸后处理可提高离体大鼠心脏缺血再灌注后心肌组织SOD的水平,改善心肌抗氧化能力,减轻心肌细胞线粒体损伤。

Objective To explore the antioxidative effect of omega-3 fatty acids postconditioning on myocardial ischemia reperfusion injury in isolated working hearts of rats.Methods Sixty Sprague-Dawley rats were randomly divided into 4 groups.Langendorff model of isolated rat heart was constructed and group A was perfused for 150 minutes without cardioplegia ischemia.the other three groups（B,C and D）were subjected to 30 minutes of ischemia and 90 minutes of reperfusion after perfused for 30 minutes.At the onset of reperfusion,the process of 20 seconds reperfusion followed by a 20 seconds ischemia was repeated 4 times in group C.Group D was treated by 15 minutes of omega-3 fatty acids at the onset of reperfusion.The lever of SOD,MDA and LDH were measured after reperfusion.Finally,morphologic changes of mitochondria were observed by the method of transmission electron microscope and infarcted sizes in heart were determined by staining with TTC.Results The level of MDA and LDH were decreased siganificantly in group C and D as compared with group B（P〈0.05）,and the level of SOD was increased siganificantly in group D（P〈0.05）.The percentages of myocardial infract sizes was less in group C and D than in group B（P〈0.05）.Myocardial mitochondrial impairment was reduced siganificantly in group C and D as compared with group B.Conclusion Omega-3 fatty acids postconditioning can enhance the level of antioxidas and reduce myocardial mitochondrial impairment,which functions to protect myocardium against ischemia reperfusion injury in isolated rat heart.