摘要
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 NOS mRNA in the progress of cardiac hypertrophy. Method： SD rats were divided into control group, hypertrophy group and captopril group. The expressions of NOS mRNA in left ventricle were detected by RT-PCR in different groups at 1.2 and 4 weeks after operation. Result：①Compared with control group, SBP and LVW/BW in hypertrophy group were significantly increased at 1 w, 2 w and 4 w after operation; The expressions of eNOS mRNA were significantly reduced at 1w, 2 w and 4w postoperation; The expressions of iNOS mRNA were significantly increased at 1w and 2w postoperation,while no marked change at 4w postoperation; The expression of nNOS mRNA had no change. ②Compared with hypertrophy group, SBP and LVW/BW were significantly decreased ; The expression of eNOS reRAN was upregulated; The expression of iNOS mRAN was significantly decreased in captopril group, which were similar to those of control group. Conclusion：eNOS and iNOS maybe play a regulation role in the process of cardiac hypertrophy,and catopril could inhibit the hypertrophic response after abdominal aorta constricting which is relative with the changes of eNOS and iNOS mRNA expression.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2005年第9期544-547,共4页
Journal of Clinical Cardiology
基金
江苏省高校自然科学研究计划项目(No:OOKJB310001)
