【摘要】 目的　进一步观察卡托普利对压力负荷增加大鼠血浆醛固酮的影响 ,探讨其抗心肌纤维化的可能作用机制。方法　建立腹主动脉狭窄所致充血性心力衰竭心肌肥厚大鼠模型 ,观察左室质量指数 (LVMI) ;采用免疫组织化学染色方法观察心肌Ⅰ、Ⅲ型胶原的改变 ;采用放射免疫分析方法检测血浆醛固酮水平的改变。结果　模型组LVMI高于假手术组 (P <0 0 1) ,卡托普利组LVMI较模型组下降 (P <0 0 5 ) ;模型组Ⅰ型胶原较假手术组升高 (P <0 0 1) ,卡托普利组较模型组下降 (P <0 0 5 ) ;模型组Ⅲ型胶原较假手术组升高 (P <0 0 1) ,卡托普利组较模型组下降 (P <0 0 5 ) ;模型组血浆醛固酮水平较假手术组升高 (P <0 0 1) ,卡托普利组降低血浆醛固酮 (P <0 0 1)水平。结论　压力负荷增加大鼠血浆醛固酮水平是升高的 ;卡托普利逆转压力负荷增加大鼠心肌纤维化的作用可能与降低血浆醛固酮水平有关更多还原

【Abstract】 Objective To confirm the effect of plasma aldosterone and reversing myocardial fibrosis of congestive heart failure(CHF) with captopril and to elucidate its possible mechanism. Methods The effects of captopril on left ventricular mass index (LVMI), cardiac tissue collagen type Ⅰand Ⅲ, plasma aldosterone (Ald) in rat with myocardial hypertrophy of CHF by abdominal aortic constriction were observed. Collagen type Ⅰand Ⅲ were measured by immunohistochemistry. Aldosterone was measured by radioimmunoassay. Results LVMI of model group increased ( P <0 01, vs sham group),while LVMI of captoril group decreased ( P <0 05, vs model group).Collagen type Ⅰ of the model group increased ( P <0 01, vs sham group), while that of the captopril group decreased ( P <0 05, vs model group). Collagen type Ⅲ of the model group increased ( P <0 01, vs sham group), while that of the captopril group decreased ( P <0 05, vs model group). The plasma aldosterone of the model group increased ( P <0 01, vs sham group), while that of the captopril group decreased ( P <0 01, vs model group). Conclusion The level of plasma aldosterone in the rat with pressure overload is increased. The effect of regressing myocardial fibrosis in the rat with CHF by captopril may be related to the decrease in plasma aldosterone level.更多还原