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实验采用腹主动脉缩窄法复制大鼠心肌肥厚模型，观察心肌过氧化脂质（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）水平以及尼群地平（Ｎｉｔ）和卡托普利（Ｃａｐ）治疗的作用。结果表明：大鼠腹主动脉缩窄后，左室重量增加，同时心肌匀浆中ＬＰＯ含量增高，ＳＯＤ活性下降，经相关关系分析，ＬＶＷ／ＢＷ与心肌组织ＬＰＯ含量显著正相关，ｒ为０．７６９，而与总ＳＯＤ活性呈显著性负相关，其ｒ为０．７８５。应用Ｎｉｔ、Ｃａｐ治疗能降低心肌组织中ＬＰＯ含量，升高ＳＯＤ活性，明显阻止心肌肥厚的形成。研究结果表明，氧自由基可能参与了心肌肥厚的发生和发展
Experimental rat model of myocardial hypertrophy was induced by abdominal aorta stenosis. The levels of myocardial lipid peroxidation (LPO), superoxide dismutase (SOD) and nitric oxide (Nitrate) and cap therapy Role. The results showed that the left ventricular weight was increased after the abdominal aorta constriction in rats, while LPO content and SOD activity in myocardial homogenate increased. Correlation analysis showed that there was a significant positive correlation between LVW / BW and myocardial LPO content (r = 0 .769, but with a significant negative correlation with the total SOD activity, the r is 0.785. The application of Nit, Cap treatment can reduce the content of LPO in myocardial tissue, increase the activity of SOD and obviously prevent the formation of cardiac hypertrophy. The results show that oxygen free radicals may be involved in the occurrence and development of cardiac hypertrophy