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目的:研究一氧化氮合酶(NOS)mRNA在心肌肥厚发生发展中的作用以及卡托普利防治心肌肥厚的机制。方法:采用腹主动脉狭窄术建立压力超负荷心肌肥厚动物模型,应用RT-PCR方法于术后1、2、4周,分别检测对照组、心肌肥厚组和卡托普利组大鼠左心室心肌组织NOS mRNA表达的变化。结果:①与对照组相比,术后1、2、4周心肌肥厚组大鼠左室重/体重(LVW/BW)指标及SBP均显著升高;左心室eNOS mRNA表达降低,iNOS mRNA表达升高,nNOS mRNA表达无明显变化。②与心肌肥厚组相比,术后1、2、4周卡托普利组大鼠LVW/BW及SBP均显著降低;左心室eNOS mRNA表达升高,iNOS mRNA表达降低,接近对照组。结论: eNOS和iNOS参与心肌肥厚的发生发展过程,但二者起不同作用。卡托普利防治心肌肥厚的作用可能与其调节NOS mRNA表达密切相关。
Objective: To investigate the role of nitric oxide synthase (NOS) mRNA in the development of cardiac hypertrophy and the mechanism of captopril in preventing and treating cardiac hypertrophy. Methods: The animal model of hypertensive cardiac hypertrophy was established by abdominal aorta stenosis. The left ventricle of rats in control group, cardiac hypertrophy group and captopril group were detected by RT-PCR at 1, 2 and 4 weeks after operation. Changes of NOS mRNA expression in myocardium. Results: Compared with the control group, LVW / BW and SBP of cardiac hypertrophy group were significantly increased at 1, 2 and 4 weeks after operation; eNOS mRNA expression and iNOS mRNA expression Elevated, nNOS mRNA expression no significant change. ② Compared with myocardial hypertrophy group, the LVW / BW and SBP of captopril group were significantly decreased at 1, 2 and 4 weeks after operation; eNOS mRNA expression in left ventricle increased and iNOS mRNA expression decreased, close to the control group. Conclusion: eNOS and iNOS participate in the development of cardiac hypertrophy, but both play different roles. Captopril’s effect on prevention and treatment of cardiac hypertrophy may be closely related to its regulation of NOS mRNA expression.