内啡肽-1后处理对大鼠心肌缺血再灌注损伤的实验研究

Experimental study of endomorphin-1 postconditioning against myocardial ischemia reperfusion injury in rats

目的:观察内啡肽-1(EM-1)后处理对大鼠心肌缺血再灌注损伤的影响。方法:健康雄性SD大鼠48只,随机分为8组:假手术组(S组),缺血再灌组(IR组),缺血后处理组(IPO组),EM-1后处理10、20和50μg/kg(EM10、EM20、EM50)三组,EM-1 50μg/kg+纳洛酮3mg/kg后处理组(EM50+Nal组)、Nal后处理组(Nal组),均i.v.给药。结扎冠脉左前降支30min,再灌120min造IR模型。全程监测心率(HR)、平均动脉压(MAP)和Ⅱ导联心电图(ECG)。动脉血浆检测丙二醛(MDA)含量及乳酸脱氢酶(LDH)和超氧化物歧化酶(SOD)的活性。结果:除EM各组再灌注120min MAP外,IPO组和EM各组HR、MAP、RPP的下降程度均显著低于IR组(P<0.05,P<0.01);与IR组比较,IPO组和EM-1三个剂量组均使血浆LDH活性降低、MDA含量降低及SOD活性增加(P<0.05,P<0.01),且EM对MDA含量及SOD活性的影响呈剂量依赖;与EM50组比较,EM50+Nal组血浆LDH活性升高、MDA含量增加及SOD活性降低(P<0.05,P<0.01)。结论:EM-1后处理可能是通过激动阿片受体,引起MDA含量降低及SOD活性增加,发挥对心肌缺血再灌注损伤的保护作用。

AIM：To investigate the effects of endomorphin-1（EM-1）postconditioning in rats on myocardial ischemia reperfusion injury.METHODS：48 male Sprague Dawley rats were randomly divided into 8groups：sham group（S group）,ischemia-reperfusion group（IR group）,ischemia postconditioning group（IPO group）,EM-1postconditioning groups（10,20,50μg/kg）（EM10,EM20,EM50）,EM-1 50μg/kg＋Naloxone 3 mg/kg postconditioning（EM50＋Nal group）,Naloxone postconditioning group（Nal group）.The myocardial ischemia reperfusion injury model was established through occluding the left anterior descending branch of coronary artery for 30 min and reperfusing for 120 min in vivo.Heart rate（HR）,mean arterial pressure（MAP）,and Ⅱlead electrocardiogram were continuously monitored during the process.The arterial blood sample was obtained to measure plasma content of malondialdehyde（MDA）and the activities of lactate dehydrogenase（LDH）,superoxide dismutase（SOD）. RESULTS：In addition to the MAP of reperfusion120 min in EM-1groups,the HR,MAP,RPP of IPO and EM-1groups were significantly lower than IR group（P〈0.05,P〈0.01）.Compared with IR group,the activity of LDH and content of MDA were decreased and the activity of SOD was increased（P〈0.05,P〈0.01）in IPO and EM-1groups after reperfusion.EM-1produced a dose-related effect on the content of MDA and the activity of SOD.The activity of LDH and content of MDA were higher and the activity of SOD was lower（P〈0.01）in EM50＋Nal group than in EM50 group after reperfusion.CONCLUSION：EM-1postconditioning may produce the cardioprotection of myocardial ischemia reperfusion injury by activating opioid receptor,reducing the MDA and increasing the SOD.