摘要
目的 :建立后负荷过高的慢性心力衰竭 (chronicheartfailure ,CHF)幼鼠实验模型 ,并探讨CHF发生发展的病理生理。方法 :腹主动脉缩窄术制备CHF模型。 4周后行超声心动图、血流动力学、心肌病理分析、心肌细胞凋亡及检测血清中脂质过氧化物 (LPO)和超氧化物歧化酶 (SOD)含量。结果 :与假手术组比较 ,CHF组左室内径及室壁厚度 ,左、右心室相对重量(LVRW ,RVRW)、收缩压 (SBP)、舒张压 (DBP)、左室收缩压 (LVSP)、左室舒张末压 (LVEDP)、凋亡指数 (AI)、LPO均显著升高 (P <0 .0 1～ 0 .0 5 ) ;左室短轴缩短率FS( % )、左室射血分数EF( % )、左室内压最大收缩率 ( +dp/dtmax、左室内压最大舒张率( -dp/dtmax、SOD均显著降低 (P <0 .0 1)。结论 :幼鼠术后 4周发生CHF。心室重构、心肌细胞凋亡及氧化应激参与CHF发生、发展的病理生理过程。
Objective:To make animal model of chronic heart failure(CHF)resulting from pressure overload in juvenile rats,and discuss its pathophysiology.Methods:The animal model of CHF was established by constriction of abdominal aorta.After four weeks of operation,the high frequency ultrasonography,the hemodynamic study,the pathologic analysis of hearts were undergone,the cardiac myocyte apoptosis,and serum contents of lipid peroxidation(LPO) and superoxide dismutase(SOD) were investigated.Results:Compared with the sham-operated group,inner diameter,wall thickness of left ventricule,LVRW,RVRW,SBP,DBP,LVSP,LVEDP,AI,LPO increased significantly( P <0.01～0.05)in CHF group.A significant decrease could be seen in EF,FS,+dp/dt max ,-dp/dt max ,SOD.Conclusion:After 4 weeks of constriction of abdominal aorta,the juvenile rats have developed CHF,the ventricular remodeling,the myocardial apoptosis and oxidative stress may take part in the pathogenesis and progression of CHF.
出处
《重庆医科大学学报》
CAS
CSCD
2004年第2期169-172,共4页
Journal of Chongqing Medical University
关键词
慢性心力衰竭
心室重构
细胞凋亡
氧化应激
幼鼠
动物模型
Chronic heart failure
Ventricular remodeling
Cardiomyocyte apoptosis
Oxidative stress
Juvenile rat
Animal model
