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采用腹主动脉缩窄法建立大鼠压力负荷性心肌肥厚模型,探讨卡托普利对大鼠肥厚心肌组织中血管紧张素Ⅱ(MAng Ⅱ)与谷胱甘肽过氧化物酶(GSH-PX)的影响.结果表明:(1)腹主动脉缩窄后4周,心脏重量、MAngⅡ水平与GSH-PX活性物显著增加,而血浆内血管紧张素Ⅱ(MAng Ⅱ)变化不明显;(2)卡托普利能够降低全心重/体重比值及MAngⅡ水平,增加GSH-PX活性.提示心脏局部肾素-血管紧张素系统(RAS)参与心肌肥厚的形成,卡托普利能够抑制MAngⅡ生成,提高心肌抗氧化能力,保护心肌细胞,减少心肌损害.
To investigate the effect of captopril on angiotensin Ⅱ (MAng Ⅱ) and glutathione peroxidase (GSH-PX) in hypertrophic myocardium of rats by using abdominal aorta constriction method. ). The results showed that: (1) The cardiac weight, MAngⅡlevel and GSH-PX activity increased significantly at 4 weeks after abdominal aorta constriction, while there was no obvious change in MAng Ⅱ (2) ) Captopril decreased cardiac full-body-to-body weight ratio and MAngⅡlevel and increased GSH-PX activity, suggesting that cardiac renin-angiotensin system (RAS) is involved in cardiac hypertrophy. Captopril can inhibit the formation of MAngⅡ , Improve myocardial antioxidant capacity, protect myocardial cells, reduce myocardial damage.