脑利钠肽后处理对在体大鼠缺血再灌注后心肌损伤的影响

The protection effect of BNP postconditioning on rat heart with ischemia-reperfusion injury in vivo

目的探讨脑利钠肽(BNP)后处理对在体大鼠心肌缺血再灌注损伤心肌的保护作用。方法 24只雄性Sprague-Dawley大鼠,随机分为:(1)假手术组(SHAM组):只开胸,不结扎冠状动脉;(2)缺血再灌注组(I/R组):结扎冠状动脉左前降支45 min,再灌注3 h;(3)脑利钠肽组(BNP组):结扎冠状动脉左前降支45 min,再灌注3 h,在再灌注前10 min,开始静脉予BNP 0.01μg/(kg.min),BNP静脉恒速维持至再灌注结束。用2,3,5,氯化三苯基四氮唑检测缺血再灌注心肌的梗死面积,用TUNEL方法检测缺血再灌注心肌的凋亡,检测心肌组织超氧化物歧化酶(SOD)、丙二醛(MDA)的浓度以评估缺血再灌注心肌活性氧的水平。结果 SHAM组心肌无梗死,I/R组的大鼠梗死面积为(44.02±10.15)%,BNP组的梗死面积为(21.53±9.08)%(P<0.05)。SHAM组、BNP组与I/R组的心肌细胞凋亡指数分别为(3.13±1.62)%、(19.45±9.62)%和(38.46±12.31)%(P<0.05)。与I/R组相比,BNP组的缺血再灌注心肌组织中MDA减少(P<0.05),而SOD增多(P<0.05)。结论 BNP后处理能减少在体大鼠缺血再灌注的心肌损伤,其机制与其减少心肌缺血再灌注损伤导致的心肌细胞凋亡及降低心肌缺血再灌注损伤时的活性氧水平相关。

Objective To study the protective effect of B-type natriuretic peptide（BNP） postconditioning on rat heart with ischemia-reperfusion in vivo. Methods Twenty-four male Sprague-Dawley rats were randomly divided into 3 groups： sham operation（SHAM） group,ischemia-reperfusion（I/R） group,and B-type natriuretic peptide（BNP） group.Rat model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 45 minutes and subsequent reperfusion for 180 minutes.The heart infarct size was determined with TTC staining.The myocardial cell apoptotic index was determined with terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end-labeling（TUNEL） method.The MDA and SOD in rat myocardium were assessed 3 hours after reperfusion. Results There was no myocardial infarction in SHAM group,while the cardiac infarct size was（21.53±9.08）% and（44.02±10.15）% in BNP group and I/R group,respectively,with significant differences revealed among the 3 groups（P0.05）.Meanwhile,the apoptotic index was（3.13±1.62）%,（19.45±9.62）% and（38.46±12.31）% in SHAM,BNP and I/R group respectively,with significant differences among the 3 groups（P0.05）.Significant reduction of MDA and elevation of SOD was observed in BNP group after reperfusion,when comparing with that in I/R group（P0.05）. Conclusion BNP postconditioning protects I/R myocardium via attenuating cardiomyocyte apoptosis and inhibiting the I/R-induced production of reactive oxygen species（ROS）.