【摘要】 目的 :研究氧化应激对心衰心肌细胞凋亡的影响及卡维地洛的疗效。方法 :构建心衰人鼠模型 ,随机分为心衰组 ,卡维地洛组。药物干预 4周 ,测心功能指标、氧化代谢指标、心肌细胞凋亡率 (AI)。结果 :心衰氧化应激与AI相关 ,AI与心功能恶化和度平行并与左心室质量指数 (LVMl)有关 ,(P均 <0 .0 5 ) ;卡维地洛改善心功能 ,纠正氧化失恒 ,降低LVMI、右心室质量指数 (RVMI) ,AI下降 (P均 <0 .0 5 )。结论 :氧化应激促进心肌细胞凋亡 ,细胞凋亡参与心室重构并提示心衰预后。卡维地洛改善心功能 ,机制可能与其抗氧化应激、抗细胞凋亡、逆转心室重构有关更多还原

【Abstract】 Objective:To investigate the influence of oxygen stress on the level of cardiac apoptosis index(AI) in chronic congestive heart failure rats,and to intervene with the third-generation blocker-carvedilol to elucidate its mechanism.Methods:8 weeks after partially banding abdominal aortic artery,20 Wister rats were randomly assigned into two groups:①heart failure group( n =10);②carvedilol group( n =10).Meanwhile,sham-operated rats( n =10) were established as a control group.After 4 weeks of remedy,hemodynamic parameters,ventricular mass index(LVMI and RVMI),oxygen stress including superoxide dismutase (SOD) and malondialdehyde (MDA),and myocardiac apoptosis were studied.Results:①Compared with sham-operated rats,all the hemodynamics were deteriorated,and LVMI and RVMI were increased significantly ( P <0.01～0.05).Plasma MDA was on rise while SOD decreased ( P <0.01),and cardiac apoptosis index was risen to 48.89% in heart failure rats ( P <0.001).②LVMI was positively related to the index of apoptosis, r =0.767 ( P <0.01).In addition,myocardial apoptosis level was positively associated with plasma MDA but negatively with SOD activity, r =0.701,-0.636( P <0.05),respectively.Apoptosis was paralleled with worsening heart function ( P <0.001～0.05).③After carvedilol therapy,LVMI and RVMI decreased and SOD and MDA improved( P <0.01～0.05).Heart function was also ameliorated,including systolic and diastolic function( P <0.01～0.05).Moreover,cardiac apoptosis decreased significantly( P <0.01).Conclusion:Oxygen stress may be critical for activation of cardiac apoptosis in the over-loaded heart.Apoptosis involves in ventricular remodeling,predicting the prognosis of heart failure.Carvedilol can ameliorate heart function,whose mechanism may be in its improvement of oxygen stress,and inhibition of cardiac apoptosis and reversion of ventricular remodeling.更多还原