脑利钠肽后处理能减少在体大鼠缺血再灌注后的心肌损伤

目的 通过建立在体大鼠心肌缺血再灌注模型，在大鼠心肌缺血后给予脑利钠肽，探讨脑利钠肽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Sprague-Dawley（SD）大鼠，雄性，随机分为：（1）假手术组（SHAM）：只开胸，不结扎冠状动脉；（2）缺血再灌注组（I/R）：结扎冠状动脉左前降支45分钟、再灌注 3小时；（3）脑利钠肽组（BNP）：结扎冠状动脉左前降支45分钟、再灌注 3小时，在再灌注前10分钟、开始静脉予以BNP 0.01µg·kg - 1·min - 1， 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(triphenyltetrzolium chloride, TTC)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SOD、MDA的浓度以评估缺血再灌注心肌活性氧的水平。结果 假手术组心肌无梗死，缺血再灌注组的大鼠心梗面积为（44.02±10.15）%，脑利钠肽组的心梗面积为（21.53±9.08）%(P<0.05)。假手术组、BNP组与缺血再灌注组的心肌细胞凋亡指数分别为(3.13±1.62)%、(19.45±9.62)%、(38.46±12.31)% (P<0.05)。与缺血再灌注组相比，BNP组的缺血再灌注心肌组织中MDA减少(P<0.05)、而SOD的增多(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。

THE PROTECTION EFFECT OF BNP POSTCONDITIONING ON RAT HEART SUFFERING FROM ISCHEMIA-REPERFUSION INJURY IN VIVO

Objective To study the protection effect of B-type natriuretic peptide (BNP) postconditioning on rat heart suffering from ischemia-reperfusion in vivo．Methods 24 male Sprague-Dawley rats weighing (250±50)g were randomly divided into 3 groups: sham operation group(SHAM),ischemia-reperfusion group(I/R), B-type natriuretic peptide group(BNP).A rat model in vivo of myocardial ischemia-reperfusion injury was established by ligating the left anterior descending coronary artery for 45 minutes and then 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. And the level of MDA and SOD in rat myocardium were detected after reperfusion for 3 hours. Results There was no infarct area in sham group, the cardiac infarct size of BNP group was （21.53±9.08）% ,while the I/R group’s infarct size was（44.02±10.15）% (P<0.05). The apoptotic index of SHAM,BNP and I/R group were (3.13±1.62)%、(19.45±9.62)%、(38.46±12.31)%, respectively(P<0.05). Comparing with the I/R group, the level of MDA in myocardium after reperfusion decreased (P<0.05), while the level of SOD increased (P<0.05). Conclusions BNP postconditioning has protective effect on I/R myocardium, which may be associated with its attenuating cardiomyocyte apoptosis and inhibiting the production of Reactive Oxygen Species (ROS) induced by I/R injury.