卡托普利对压力负荷增加大鼠心肌Ⅰ和Ⅲ型胶原的影响

EFFECT OF CAPTOPRIL ON MYOCARDIAL COLLAGEN TYPE Ⅰ AND TYPE Ⅲ IN RAT WITH PRESSURE OVERLOAD

目的 进一步观察卡托普利抗心肌纤维化的作用及其可能机制。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（ｌｅｆｔｖｅｎｔｒｉｃｕｌａｒ ｍａｓｓｉｎｄｅｘ，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，并采用放射免疫分析方法检测血浆和心肌血管紧张素Ⅱ（ａｎｇｉｏｔｅｎｓｉｎ Ⅱ，ＡｎｇⅡ） 水平。结果 模型组ＬＶＭＩ明显高于假手术组（ Ｐ ＜ ０．００１），卡托普利组ＬＶＭＩ与模型组比较有明显下降（ Ｐ ＜０ ．０５）；模型组Ⅰ型胶原较假手术组显著升高（ Ｐ＜ ０．０１） ，卡托普利组较模型组明显下降（ Ｐ＜ ０ ．０５）；模型组Ⅲ型胶原与假手术组比较有显著升高（ Ｐ＜０ ．０１），卡托普利组较模型组显著下降（ Ｐ＜ ０ ．０５）；模型组血浆和左室心肌ＡｎｇⅡ水平较假手术组显著升高（ Ｐ＜ ０．００１） ，卡托普利组明显降低血浆ＡｎｇⅡ（ Ｐ＜ ０ ．０１） 和左室心肌ＡｎｇⅡ水平（ Ｐ＜ ０．００１） 。结论 心肌纤维化是腹主动脉狭窄所致充血性心力衰竭心肌肥厚的１ 个重要的病理改变，卡托普利具有逆转充血性心力衰竭心肌纤维化的作用，该作用可能与降低循环和局部ＡｎｇⅡ水平有关。

ObjectiveTo confirm the effect of reversing myocardial fibrosis of congestive heart failure(CHF) with captopril and to elucidate its possible mechanism. MethodsObservation of effects of captopril on left ventricular mass index (LVMI), cardiac tissue collagen type Ⅰand Ⅲ , circulating angiotensinⅡ(AngⅡ) and left ventricular tissue AngⅡ in rat with myocardial hypertrophy of CHF by abdominal aortic constriction. Collagen type Ⅰand Ⅲ were measured by immunohistochemistry. Ang Ⅱwas measured by radioimmunoassay. ResultsLVMI of model group was increased (P< 0.001 ,vs control group),while LVMI of the captoril group was decreased (P< 0.05 ,vs model group).Collagen type Ⅰof the model group was increased (P< 0.01 , vs sham group), while that of the captopril group was decreased (P< 0.05 , vs model group). Collagen type Ⅲ of the model group was increased (P< 0.01 , vs sham group), while that of the captopril group was decreased (P< 0.05 , vs model group). The plasma and myocardial AngⅡ of the model group were increased (P< 0.001 , vs sham group), while those of the captopril group were decreased (P< 0.01 and P< 0.001 , vs model group).ConclusionMyocardial fibrosis is an important pathological change in rat with myocardial hypertrophy of CHF. Captopril is effective in regressing myocardial fibrosis of CHF. The effect may be related to the decreasing in circulating or local AngⅡ level.