摘要
目的:探讨促红细胞生成素(EPO)对大鼠心肌缺血再灌注损伤(MIRI)的保护作用及其机制。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MIRI模型。将50只SD大鼠随机分为假手术组、缺血再灌注组、EPO100U/kg治疗组、EPO1000U/kg治疗组、EPO5000U/kg治疗组5组,每组10只。连续监测肢体Ⅱ导联心电图记录再灌注时心律失常情况;测定再灌注末血清磷酸肌酸激酶同工酶(CK MB),心肌丙二醛(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;观察心肌超微结构改变。结果:EPO显著降低再灌注室性心律失常的发生;减少再灌注末血清CK MB和心肌MDA含量,提高心肌GSH PX、CAT、Na+K+ATP酶和Ca2+ATP酶的活性;明显减轻缺血再灌注对心肌超微结构的损伤。对心肌SOD活性无影响。结论:EPO对大鼠MIRI有明显的保护作用,其机制可能与减轻氧自由基及钙超载损害有关。
Objective: To explore the effects of erythropoietin on myocardial ischemia- reperfusion injury in rats. Methods: The left anterior descending coronary artery was ligated for 30 minutes and then loosed for 120 minutes to establish the rat model of myocardial ischemia-reperfusion injury. 50 SD rats were randomly divided into five groups: sham-operation,ischemia-reperfusion,EPO 100 U/kg,EPO 1000 U /kg and EPO 5000 U/kg. During the processes, lead Ⅱ ECG was traced continuously to note the arrhythmia caused by reperfusion;the levels of serum creatine phosphokinase isoenzyme (CK-MB),myocardial malonaldehyole (MDA) 、superoxide dismutase (SOD)、glutathione peroxidase ( GSH-PX)、catalase (CAT)、Na + -K +-ATPase and Ca 2+-ATPase were detected at reperfusion 120 min. And the changes of myocardial ultrastructures were observed. Results: Erythropoietin significantly reduced the incident of ventricle arrhythmia caused by reperfusion;reduced serum CK-MB and myocardial MDA content ,enhanced the activity of myocardial GSH-PX,CAT Na +-K +-ATPase,Ca 2+-ATPase at reperfusion 120 min; markedly attenuated injury of the myocardial ultrastructures caused by the ischemia- reperfusion. Erythropoietin did not change the activity of myocardial SOD. Conclusion: Erythropoietin has protective effects on myocardial ischemia- reperfusion injury in rats,and the mechanism may be related to relieving the injury caused by oxygen free radical and calcium overload.
出处
《医学研究生学报》
CAS
2005年第4期338-342,共5页
Journal of Medical Postgraduates