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目的:观察辛伐他汀对心力衰竭(心衰)家兔左室收缩功能和交感活性的影响,以阐明辛伐他汀改善非缺血性心衰心功能的可能机制。方法:30只家兔随机分为3组:假手术组(10只)、心衰组(10只)、辛伐他汀干预组(10mg.kg-1.d-1,10只);心衰组和辛伐他汀干预组家兔应用超容量负荷联合压力负荷建立非缺血性心衰模型,共观察7周。利用左心导管术和心脏多谱勒观察家兔血流动力学和心脏功能的变化,采用酶联免疫吸附法测定血浆脑钠肽(BNP)、去甲肾上腺素(NE)水平,以及蛋白免疫印迹法检测心肌组织蛋白激酶A(PKA)、受磷蛋白(PLB)及第16位丝氨酸磷酸化受磷蛋白(Pser16-PLB)的蛋白表达水平。结果:①与心衰组比较,辛伐他汀干预组家兔左室舒张末压、心率、血浆BNP和NE水平明显降低(P<0.05),而左室射血分数(EF)明显增加(P<0.05);②辛伐他汀干预组家兔心肌组织PKA和Pser16-PLB表达水平较心衰组家兔明显降低(P<0.05),2组间总PLB表达无明显差别。结论:辛伐他汀具有抗交感作用,是其延缓非缺血性心衰左室收缩功能减退的可能机制之一。
Objective: To observe the effect of simvastatin on left ventricular systolic function and sympathetic activity in rabbits with heart failure (CHF), so as to clarify the possible mechanism of simvastatin in improving cardiac function in non-ischemic heart failure. Methods: Thirty rabbits were randomly divided into three groups: sham operation group (n = 10), heart failure group (n = 10), simvastatin intervention group (10 mg.kg-1.d- The rabbits in the simvastatin group and the simvastatin group were subjected to a non-ischemic heart failure model by overloading the combined stress load for a total of 7 weeks. Left ventricular catheterization and cardiac Doppler were used to observe the changes of hemodynamics and cardiac function in rabbits. Plasma BNP and NE levels were measured by enzyme-linked immunosorbent assay The expression of protein kinase A (PKA), phospholamban (PLB) and Pser16-PLB protein in myocardium were detected by Western blotting. Results: Compared with heart failure group, left ventricular end-diastolic pressure, heart rate, plasma BNP and NE levels were significantly decreased (P <0.05) and left ventricular ejection fraction (EF) significantly increased in simvastatin intervention group <0.05). ② The expression levels of PKA and Pser16-PLB in rabbits in simvastatin treatment group were significantly lower than those in HF group (P <0.05). There was no significant difference in total PLB expression between the two groups. Conclusion: Simvastatin has anti-sympathetic effect, which is one of the possible mechanisms of its delay in left ventricular systolic dysfunction in non-ischemic heart failure.