高压负荷性心衰幼鼠病理生理及卡维地洛的干预

目的：探讨后负荷过高的幼鼠慢性心力衰竭（chronic heart failure，CHF）发生发展的病理生理及卡维地洛的干预。方法：腹主动脉缩窄术制备幼鼠CHF模型。术后4周随机分3组：假手术对照组、CHF组、卡维地洛组。直接灌胃给药，8周后行血流动力学、心肌病理分析、心肌细胞凋亡及其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，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〈0．01—0．05）；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〈0．01）。与CHF组比较，卡维地洛组LVRW、RVRW、SBP、DBP、LVSP、LVEDP、AI、LPO显著下降，＋dp／dtmax、-dp／dtmax、SOD显著升高（P〈0．01）。结论：心室重构、心肌细胞凋亡及氧化应激参与幼鼠CHF发生、发展的病理生理过程，而卡维地洛能延缓、抑制这一过程。

Pathophysiological changes of chronic heart failure resulting from pressure overload in juvenile rats and the interference of carvedilol

Objective: To explore the pathophysiological changes of chronic heart failure resulting from pressure overload in juvenile and the effects of carvedilol. Methods: The animal model of CHF was established by constriction of abdominal aorta. Four weeks after operation, the rats were randomly divided into 3 groups: sham-operated group, CHF group, carvedilol group. Carvedilol was administered by direct gastric gavage. Eight weeks after operation, the hemodynamic analysis, the pathologic analysis of hearts and the cardiac myocyte apoptosis analysis were performed. The serum contents of lipid pereoxidation(LPO) and superoxide dismutase(SOD) were detected. Results: Compared with the sham-operated group, SBP, DBP, LVSP, LVEDP, LVRW, RVRW, LPO, AI were all significantly increased(P < 0.01) in CHF group. A significant decrease could be seen in dp/dtmax, -dp/dtmax, SOD in CHF group. A significant decrease could be seen in SBP, DBP, LVSP, LVEDP, LVRW, RVRW, LPO, AI in carvedilol group compared with CHF group. While a significant increase could be seen in dp/dtmax, -dp/dtmax and SOD(P < 0.01). Conclusion:The ventricular remodeling, the myocardial apoptosis and oxidative stress may take part in the pathogenesis and progression of CHF, which might be inhibited by carvedilol.