【摘要】 目的:探讨早期卡托普利治疗抑制左室肥厚的机制.方法:♂SHR宫内期给药(100 mg·kg^-1·d^-1)到16周,40周处死,测定收缩压,左室重与体重比,左室c-myc和c-fos表达量（Northern杂交）.结果:治疗明显降低血压,停药后24周,仍维持较低血压（20.9±1.2vs对照SHR 28.3±1.3 kPa,P<0.01）并抑制左室肥厚,心肌c-myc表达明显减少（0.57±0.13 vs对照SHR 2.07±0.16,c-myc mRNA/18S rRNA,P<0.01）,c-fos表达无变化.结论:卡托普利持久地阻止高血压形成,抑制左室肥厚.后者可能是抑制c-myc表达结果,治疗不改变c-fos表达.更多还原

【Abstract】 AIM:To explore the mechanisms by which angiotensin converting enzyme inhibitor (ACEI) prevents the development of left ventricular hypertrophy (LVH). METHODS: Captopril (Cap 100 mg.kg-1.d-1) was given orally to spontaneously hypertensive rats from intrauterine period to 16 wk of age. Ex-periments were performed at 40 wk of age. SBP, left ventricular weight to body weight ratio(LVW/BW) were assessed. The levels of c-myc and c-fos mRNA in the left ventricle were measured by Northern blot. RESULTS: Early-onset Cap therapy significantly decreased SBP. After discontinuance of treatment for 24 wk, SBP of SHRcap was still maintained at a lower level. LVW/BW in SHRcap was markedly reduced. The expression of myocardial c-myc mRNA was decreased by 72 % in SHRcap compared with that in the untreated SHR, but the expression of myocardial c-fos mRNA was not different between the untreated SHR, SHRcap,and WKY rats. CONCLUSION: Early Cap treatment may permanently prevent the development of hypertension, inhibit LVH. Furthermore, the prevention of LVH is associated with a decrease in c-myc mRNA levels, and the development and regression of left ventricular hypertrophy may be irrelevant to c-fos expression.更多还原