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目的观察外源性肝细胞生长因子(HGF)对心肌梗死后心肌细胞凋亡及左室重塑的影响。方法56只新西兰兔随机分为4组 :假手术组、假手术 +HGF组、对照组和干预组。结扎左冠状动脉前降支复制急性心肌梗死模型。干预组静脉注射HGF2mg/kg/12h ,4周后测心功能、左室重塑指标 ,取出心脏 ,梗死区/缺血区重量比为梗死范围。TUNEL法染色检测细胞凋亡。结果与假手术组相比 ,对照组的左室舒张末容积、左室相对重量、左室壁厚度均显著升高 (P<0.05～0.01) ,左室短轴收缩率(LVFS)、左室射血分数(LVEF)均显著降低 (P<0.01)。与对照组相比 ,HGF干预组LVSV、LVEDV显著降低 ;LVFS及LVEF均显著升高。HGF干预组细胞凋亡率、心肌梗死范围均低于对照组 (P<0.01)。左室腔直径与心肌细胞凋亡率呈正相关 (r=0.801 ,P<0.01)。结论HGF能减少心肌梗死范围、降低心肌细胞凋亡率并能限制AMI后的左室重塑 ,改善心功能 ,其作用机制可能与其抗心肌细胞凋亡有关
Objective To observe the effect of exogenous hepatocyte growth factor (HGF) on cardiomyocyte apoptosis and left ventricular remodeling after myocardial infarction. Methods 56 New Zealand white rabbits were randomly divided into 4 groups: sham operation group, sham operation + HGF group, control group and intervention group. Ligation of left anterior descending coronary artery for acute myocardial infarction model. The intervention group received intravenous injection of HGF 2 mg / kg / 12 h. After 4 weeks, cardiac function and left ventricular remodeling index were taken and the heart was removed. The weight ratio of infarct area to ischemic area was the infarction area. TUNEL staining was used to detect apoptosis. Results Compared with the sham operation group, left ventricular end diastolic volume, left ventricular relative weight and left ventricular wall thickness were significantly increased (P <0.05 ~ 0.01), left ventricular short axis systole (LVFS) The ejection fraction (LVEF) decreased significantly (P <0.01). Compared with the control group, the LVSV and LVEDV in the HGF intervention group were significantly decreased, and both LVFS and LVEF were significantly increased. HGF intervention group apoptosis rate, myocardial infarction range were lower than the control group (P <0.01). The diameter of left ventricular cavity was positively correlated with the rate of cardiomyocyte apoptosis (r = 0.801, P <0.01). Conclusion HGF can reduce the range of myocardial infarction, reduce the rate of myocardial apoptosis and can limit left ventricular remodeling after AMI and improve cardiac function, the mechanism may be related to its anti-myocardial cell apoptosis