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目的探讨坎地沙坦改善慢性心衰大鼠心室重塑和抑制心肌纤维化(myocardial fibrosis,MF)可能的作用机制。方法采用肾上腹主动脉缩窄法制作的雄性Wistar大鼠慢性心衰模型,随机分为心衰组(HF组)及药物组(Drug组),另有假手术组(Sham组)作为对照。给药组大鼠予以坎地沙坦2mg·kg-1·d-1灌胃,HF组和Sham组用等体积生理盐水灌胃。4周后检测血流动力学参数,左室心肌胶原形态,左室质量指数(LVMI)、胶原容积分数(CVF)和血管周围胶原面积(PVCA),免疫组化法检测心室肌中转化生长因子(TGF-β1)、结缔组织生长因子(CTGF)表达。结果给药组大鼠与心衰组相比LVEDP降低,±dp/dtmax增高。LVMI,CVF,PVCA降低。TGF-β1,CTGF表达显著降低。结论坎地沙坦明显改善心室重塑、抑制MF,提高心功能。此作用可能与降低CTGF,TGF-β1表达有关。
Objective To investigate the possible mechanism of candesartan in improving ventricular remodeling and inhibiting myocardial fibrosis (MF) in chronic heart failure rats. Methods Chronic heart failure model of male Wistar rats were made by the method of renal artery aortic constriction. They were randomly divided into heart failure group (HF group) and drug group (Drug group), sham operation group (Sham group) . Rats in the treatment group were given candesartan 2mg · kg-1 · d-1 gavage, HF group and Sham group with an equal volume of normal saline. Four weeks later, hemodynamic parameters, left ventricular myocardial collagen morphology, left ventricular mass index (LVMI), collagen volume fraction (CVF) and perivascular collagen area (PVCA) were measured. Immunohistochemistry was used to detect the expression of transforming growth factor (TGF-β1), connective tissue growth factor (CTGF) expression. Results Compared with heart failure group, LVEDP decreased and ± dp / dtmax increased in the treated group. LVMI, CVF, PVCA reduced. TGF-β1, CTGF expression was significantly reduced. Conclusion Candesartan significantly improves ventricular remodeling, inhibits MF and improves cardiac function. This effect may be related to decreasing the expression of CTGF and TGF-β1.