卡托普利对压力负荷增加大鼠心肌Ⅰ和Ⅲ型胶原的影响

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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。 Objective To further observe the anti-myocardial fibrosis of captopril and its possible mechanism. Methods The rat model of myocardial hypertrophy caused by abdominal aortic stenosis was established and the left ventricular mass index (LVMI) was observed. The changes of myocardial collagen types Ⅰ and Ⅲ were observed by immunohistochemical staining and radioimmunoassay Analytical methods were used to detect plasma and myocardial angiotensin Ⅱ (AngⅡ) levels. Results The LVMI in model group was significantly higher than that in sham operation group (P <0.001), and the LVMI in captopril group was significantly lower than that in model group (P <0.05). The type Ⅰ collagen in model group was significantly higher than that in sham operation group (P <0.01), the captopril group was significantly lower than the model group (P <0 .05), the type Ⅲ collagen in the model group was significantly higher than that in the sham operation group (P <0.01) The level of AngⅡ in plasma and left ventricular myocardium in model group was significantly higher than that in sham operation group (P <0.001), while the level of plasma AngⅡ in captopril group was significantly lower than that in model group (P <0.05) (P <0.01) and left ventricular Ang Ⅱ level (P <0.001). Conclusions Myocardial fibrosis is an important pathological change of cardiac hypertrophy caused by abdominal aortic stenosis. Captopril can reverse myocardial fibrosis in patients with congestive heart failure, which may be related to the decrease of circulating AngⅡ Horizontal related.
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