地塞米松对I/R心肌梗死面积及抗氧自由基酶的影响

目的:探讨地塞米松预处理对大鼠缺血 - 再灌注(I/R)心肌梗死面积的影响及机制. 方法: SD大鼠随机分成地塞米松组、对照组,分别予地塞米松和生理盐水预处理.预处理后构建Langendorff离体心脏I/R动物模型,缺血30 min后再灌注60 min,测定心肌丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化酶(GSH-Px)水平;TTC法测定心肌梗死面积;观察心肌超微结构变化.结果:与对照组相比,地塞米松组MDA水平显著降低(P＜0.01),SOD、CAT、GSH-Px水平升高(P＜0.05);心肌梗死面积明显缩小(P＜0.01).结论:地塞米松可减轻缺血再灌注后心肌梗死面积及心肌超微结构的损伤,其机制可能通过升高心肌组织抗氧自由基酶的水平、抑制脂质过氧化反应有关.

The Effect of Dexamethasone on Sizes of Infarction and Contents of MDA, SOD, CAT, GSH-Px in Rat Hearts Induced by Ischemia/reperfusion

Objective: To explore the effect of dexamethasone(DEX) preconditioning on the myocardial infarction sizes caused by ischemia/reperfusion(I/R) and its mechanism.Methods: Forty-eight Sprague-Dawley rats were divided randomly into DEX and control(CON) groups,of which the rats were pretreaded with DEX(DEX group) or sodium chloride(CON group) before their hearts were separated for Langendorff perfusion and ischemia/reperfusion.The 30-minute ischemia was caused by triphenyltetrazolium chloride(TTC) and followed by 60-minute reperfusion.The myocardial infarction sizes were measured and the myocardial ultrastructures were examined afterwards.The reperfusion caused myocardial injury,malonaldehyole(MDA),superoxide dismutase(SOD),catalase(CAT),and glutathione peroxidase(GSH-Px) were detected.Results: Compared with control group,the MDA was significantly lower(P<0.01) and the SOD,CAT,GSH-Px were significantly higher in group DEX(P<0.05);The sizes of infarction were reduced significantly(P<0.01).Conclusions: Dexamethasone can reduce the myocardial infarction sizes and the injury of myocardial ultrastructure during I/R.The mechanism might be the enhancement of myocardial antioxidase activity to inhibit lipid peroxidation.