电刺激小脑顶核防治心肌梗死后大鼠心肌氧化损伤

目的:研究电刺激小脑顶核(FNS)对急性心肌梗死(AMI)大鼠心肌氧化损伤的防治作用机制.方法:随机将大鼠分为AMI、FNS AMI、毁损小脑顶核(FNL) AMI组,于左冠状动脉结扎术后24h进行心肌梗死面积、血清乳酸脱氢酶(LDH)和肌酸激酶(CK)活性、心肌组织丙二醛(MDA)含量和总抗氧化能力(TAOC)及超氧化物歧化酶(SOD)活性测定.结果:与MI组比较,FNS AMI组LDH、CK活性,MDA含量,心肌梗死面积显著减少(P＜0.01);TAOC及SOD活性显著升高(P＜0.01).FNL AMI组与AMI组以上指标比较无显著性差异(P＞0.05).结论:FNS可减轻心肌梗死后大鼠心肌损伤,减小心肌梗死面积;其心肌保护机制可能与其抗氧化损伤作用有关.

The preventive effect of fastigial nucleus stimulation on the oxidative damage in rats with myocardial infarction

Objective:To investigate the effect of fastigial nucleus stimulation(FNS) on preventing oxidative damage from myocardium after acute myocardial infarction in rats.Methods:Wistar rats were randomly divided into acute myocardial infarction(AMI),FNS before AMI model was made(FNS AMI),bilateral fastigial nucleus lesion(FNL) before AMI(FNL AMI) groups.At 24 hours after coronary ligation,blood samples and left ventricular myocardium were obtained for measurment of the activity of lactic dehydrogenase(LDH) and creatine phosphokinase(CK) in serum,as well as myocardial infarct size.At the same time,the malondialdehyde(MDA) level,total anti-oxidative capability (TAOC) and superoxide dismutase(SOD) activity in myocardium were measured too.Results:LDH,CK activities and MDA level in FNS AMI group were significantly lower than that in AMI group( P <0.01).The infarct size in FNS AMI group was significantly smaller than that in group AMI( P <0.01).SOD activity and TAOC were significantly increased in FNS AMI group as compared to AMI group.There was no significant difference between FNL AMI group and AMI group for all the measurements( P >0.05).Conclusion:FNS can attenuate the damage of myocardium from infarct heart and reduce myocardial infarct size.The mechanism of the protective effect coming from FNS may be related to its antioxidative role.