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目的:研究破格救心汤对心梗后心力衰竭(HF)大鼠心功能的影响及其作用机制。方法:采用阿霉素诱导法复制HF大鼠模型,随机分为模型组、破格救心汤高、低剂量组(18.66,9.33 g·kg-1)和福辛普利钠组(4.67 mg·kg-1),同时设立空白对照组。连续灌胃给药28 d。心脏超声评价各组大鼠心功能,放射免疫法测定各组大鼠血浆中的醛固酮(ALD)和血管紧张素Ⅱ(AngⅡ),并进行心肌病理学检测。结果:与空白对照组比较,模型组左室舒张末内径(LVEDd)和左室收缩末内径(LVEDs)明显增大(P<0.05),射血分数(EF)明显下降(P<0.05);与模型组比较,破格救心汤高、低剂量组均能提高HF大鼠的EF,同时能有效改善大鼠心功能并缩短LVEDd和LVEDs。模型组大鼠血浆中的ALD和AngⅡ明显高于空白对照组(P<0.05);破格救心汤高、低剂量组和福辛普利钠组均能下调HF大鼠血浆中的ALD和AngⅡ浓度(P<0.05)。模型组心肌病理学提示心肌纤维排列紊乱,染色深浅不均,可见断裂及分带现象,部分肌纤维相互分离;破格救心汤高、低剂量组和福辛普利钠组均提示心肌纤维断裂现象明显减轻。结论:破格救心汤能缩短HF大鼠的LVEDd和LVEDs,逆转心肌重构,从而改善心功能,其机制可能与降低HF大鼠血浆中肾素-血管紧张素-醛固酮系统(RAAS)的激化水平特别是ALD和AngⅡ水平,改善心脏后负荷有关。
Objective: To investigate the effect and the possible mechanism of “Xinggejiuxin Decoction” on cardiac function in heart failure rats after myocardial infarction (HF). Methods: HF model rats were induced by doxorubicin induction and were randomly divided into model group, high-dose and low-dose Xueshuixin decoction group (18.66, 9.33 g · kg -1) and fosinopril sodium group (4.67 mg · kg -1 -1), while setting up a blank control group. Continuous oral administration of 28 d. Cardiac function was evaluated by echocardiography. Plasma aldosterone (ALD) and angiotensin Ⅱ (AngⅡ) levels were measured by radioimmunoassay. Cardiomyopathological examination was performed. Results: Compared with the blank control group, the left ventricular end - diastolic diameter (LVEDd) and left ventricular end - diastolic dimension (LVEDs) of the model group increased significantly (P <0.05) and the ejection fraction (EF) decreased significantly (P <0.05). Compared with the model group, Jianqixinxin Decoction high and low dose groups can improve the EF of HF rats, improve the cardiac function and shorten the LVEDd and LVEDs. ALD and AngⅡ in the plasma of rats in model group were significantly higher than those in blank control group (P <0.05), while those in high and low doses of shangqiu xinxin group and fosinopril sodium group decreased plasma ALD and AngⅡ (P <0.05). Myocardial pathology in the model group suggested that the myocardial fibers were disordered, the depth of dyeing was uneven, the phenomenon of rupture and zonation was visible, and some muscle fibers were separated from each other. The high, low and high doses of FENGXINXIN decoction induced the obvious myocardial fiber breakage Reduce. Conclusion: Jiangeyixin Decoction can shorten the LVEDd and LVEDs of HF rats and reverse cardiac remodeling, thus improving cardiac function. The mechanism may be related to decreasing the level of plasma renin-angiotensin-aldosterone system (RAAS) in HF rats In particular, ALD and Ang Ⅱ levels improve cardiac afterload related.