目的建立大鼠急性心肌梗死(acute myocardial infarction,AMI)模型,观察AMI后卡维地洛早期处理对心梗后左室重构的影响。方法雄性Wistar大鼠60只,随机分为假手术组(n=15)、AMI组(n=15)、低剂量卡维地洛组(n=15)和高剂量卡维地洛组(n=15)。建模后2周心肌组织取材,HE、Masson染色病理学检查;免疫组织化学测定心肌组织中毛细血管及抗凋亡、凋亡蛋白表达;建模前1 d及建模后2周心脏超声检查;采用Elisa法对建模前及建模后2周血浆脑钠肽(BNP)水平测定。结果建模后2周,与AMI组比较,卡维地洛组梗死面积减小,梗死区存活心肌细胞数增加,替代性纤维化面积减小,抗凋亡蛋白bcl-xl表达增强,凋亡蛋白Bax表达降低,P<0.05;梗死区及梗死旁区心肌组织中幼稚毛细血管密度增加,上述改变在高剂量药组明显;心脏超声左室收缩末期内径(LVESD)、左室舒张末期内径(LVEDD)、室间隔厚度(IVS)直线小,心率(HR)减慢,左室射血分数(EF)值增加(P<0.05);血浆BNP水平较AMI组明显降低(P<0.05)。结论大鼠AMI后早期应用卡维地洛处理,可减少心肌细胞的凋亡及丢失,减轻AMI后心肌梗死程度,减轻左心室重构,改善AMI后左室功能,延缓心力衰竭的发生。 Objective To establish a rat model of acute myocardial infarction (AMI) and observe the effect of early treatment of carvedilol on left ventricular remodeling after AMI. Methods Sixty male Wistar rats were randomly divided into sham operation group (n = 15), AMI group (n = 15), low dose carvedilol group (n = 15) and high dose carvedilol group = 15). Myocardial tissue samples were taken 2 weeks after the model establishment, HE and Masson stained pathological examination; capillary and anti-apoptotic and apoptotic protein expression in myocardial tissue were detected by immunohistochemistry; 1 d before modeling and 2 weeks after modeling echocardiography Elisa method was used to determine plasma BNP level before and 2 weeks after modeling. Results Compared with AMI group, the infarct size of carvedilol group decreased, the number of viable myocardial cells in infarct area increased, the area of ​​alternative fibrosis decreased, the expression of anti-apoptotic protein bcl-xl increased, and apoptosis increased (P <0.05). The density of naive capillaries in the infarct area and in the para-infarct myocardium was increased, which was significantly higher in the high-dose group. The left ventricular end- systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD). The IVS was linear and the heart rate (HR) slowed down. The left ventricular ejection fraction (EF) increased (P <0.05). The plasma BNP level was significantly lower than that of AMI group (P <0.05). Conclusion Carvedilol treatment in the early AMI can reduce the apoptosis and loss of cardiomyocytes, reduce the degree of myocardial infarction after AMI, relieve left ventricular remodeling, improve left ventricular function after AMI and delay the occurrence of heart failure.