破格救心汤改善心梗后心衰大鼠心功能的作用

Study on Effect of Poge Jiuxin Decoction on Heart Failure after Myocardial Infarction in Rats

摘要:

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。

Abstract:

Objective:To study the effect and possible mechanism of Poge Jiuxin decoction(PGJXD) on heart failure(HF) after infarction induced by Yang weak and body fluid flood syndrome in rats. Method: Rat model of HF was induced by adriamycin. The model-established rats were randomized into model group,PGJXD high-dosage group(18.66 g·kg^-1),low-dosage group(9.33 g·kg^-1) and the fosinopril sodium group(4.67 mg·kg^-1). A blank control group was also set up. Drugs were given by continuous intragastric administration for 28 days. Then cardiac function of each group was evaluated by echocardiography,plasma aldosterone(ALD) and angiotensin Ⅱ(AngⅡ) levels were also examined by radioimmunoassay(RIA) in all groups,and myocardial pathology biopsy was carried out. Result: Compared with the blank group,the left ventricular end-diastolic diameter(LVEDd) and left ventricular end-systolic diameter(LVEDs) of model group increased significantly(P<0.05),ejection fraction(EF)decreased significantly(P<0.05). After given the high-dose and middle-dose of PGJXD and the fosinopril sodium, EF and cardiac function were improved. Moreover,PGJXD could effectively shorten the LVEDd and LVEDs,and fosinopril sodium did not work. RIA results showed that ALD and AngⅡ in plasma of model group was significantly higher than those in blank group(P<0.05);the high-dose and middle-dose of PGJXD and the fosinopril sodium could down-regulate the plasma ALD and AngⅡ(P<0.05). In the models, myocardial pathology investigation suggested myocardial fibers derangement,with visible dyeing depth,fracture and zoning,part of the muscle fibers were separated from each other. Compared with the model group,the high-dose and middle-dose of PGJXD and the fosinopril sodium showed obvious reduced myocardial fiber breakage. Conclusion: PGJXD can shorten the LVEDd and LVEDs,and thus reverse myocardial remodeling and strength the cardiac function. The mechanism may be related to decrease in plasma ALD and AngⅡ and reduce in renin-angiotensinrenin-angiotensinaldosterone system(RAAS) activity thus to improve cardiac afterload in HF Rats.