摘要
目的:观察促红细胞生成素(erythropoietin,EPO)对大鼠心肌缺血-再灌注心律失常的影响并探讨其作用机制。方法:采用结扎左冠状动脉前降支30min再灌注120min的方法建立大鼠心肌缺血-再灌注损伤模型。将60只SD大鼠随机分为3组(假手术组、缺血-再灌注组、EPO治疗组)。连续监测肢体Ⅱ导联心电图记录再灌注心律失常情况;测定再灌注末心肌组织丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、Na+-K+-ATP酶和Ca2+-ATP酶的变化。结果:EPO降低再灌注室性心律失常的发生率与持续时间,使心律失常评分显著降低;EPO减少再灌注末心肌MDA含量,提高心肌GSH-Px、CAT、Na+-K+-ATP酶和Ca2+-ATP酶的活性,对心肌SOD活性无影响。结论:EPO具有抗心肌缺血-再灌注室性心律失常的作用,其机制可能与减轻氧自由基及钙超载的损害有关。
Objective To observe the effects of erythropoietin on arrhythmia induced by myocardial isehemia-reperfusion in rats. Methods The rat model of myocardial isehemia-reperfusion injury（IRI） was set up by ligating of left anterior descending coronary artery for 30 minutes and then loosing for 120 minutes, Sixty SD rats were randomly divided into three groups： sham-operation group（ n = 20）, ischemia-reperfusion group（ n = 20） and EPO group（ n = 20） , During the experimental procedures, lead Ⅱ ECG was traced continuously for the arrhythmia induced by ischemia or reperfusion. The levels of myocardial malonaldehyole （MDA）, superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, eatalase （CAT）, Na^＋-K^＋-ATPase and Ca^2＋-ATPase were detected at 120 min after reperfusion. Results Erythropoietin decreased the incidence and the duration of ventricle arrhythmia induced by reperfusion, resulting in the scores of arrhythmia decrease significantly. Erythropoietin reduced myocardial MDA content, enhanced the activity of myocardial GSH-Px, CAT, Na^＋-K^＋-ATPase, Ca^2＋-ATPase at 120 min after reperfusion but didn＇t affect the activity of myocardial SOD. Conclusion Erythropoietin may effectively prevent ventricle arrhythmia induced by myocardial ischemia-reperfusion, and its mechanism may be related to the decrease of the injury caused by oxygen free radical and calcium overload.
出处
《实用医学杂志》
CAS
2006年第9期993-995,共3页
The Journal of Practical Medicine
