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背景心力衰竭(心衰)是不同原因所致的多种心脏病发展的最终结果,目前国内尚没有关于心衰时心肌钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)的变化以及辛伐他汀长期干预进而预防心衰的报道。目的探讨家兔心衰时心肌CaMKⅡ蛋白表达及活性的改变及辛伐他汀长期干预的意义。方法家兔18只随机分为3组:假手术组、心衰组和辛伐他汀组[10mg/(kg·d)],每组6只,通过超容量负荷联合压力负荷建立家兔心衰模型,于术后7周观察左心室结构、血流动力学的变化及CaMKⅡ的表达和活性的改变。结果心衰组左心室质量指数(LVMI)增加[假手术组(1.3±0.1)比心衰组(3.6±0.1)g/kg]、左室舒张末径(LVEDD)增加[假手术组(13.3±1.8)比心衰组(21.4±2.5)mm]、左室后壁厚度(LVPW)增加[假手术组(2.0±0.2)比心衰组(2.9±0.8)mm]、左心室舒张末压(LVEDP)增加[假手术组(-1.5±0.5)比心衰组(23.0±2.4)mmHg](P<0.05);心衰组左心室缩短率(LVFS)减少[假手术组(37.8±3.6)%比心衰组(17.4±3.1)%],左室射血分数(LVEF)下降[假手术组(71.9±4.6)%比心衰组(38.5±6.1)%](P<0.05)。辛伐他汀能降低LVMI[(2.1±0.1)比心衰组(3.6±0.1)g/kg]、LVEDD[(17.6±1.9)比心衰组(21.4±2.5)mm]、LVPW[(2.1±0.5)比心衰组(2.9±0.8)mm]、LVEDP[(2.2±0.8)比心衰组(23.0±2.4)mmHg](P<0.05),提高LVFS[(33.8±2.5)%比心衰组(17.4±3.1)%]及LVEF[(63.2±3.5)%比心衰组(38.5±6.1)%](P<0.05)。心衰组CaMKⅡ蛋白表达上调(1.5±0.1比假手术组:0.9±0.1),活性上调[(3.5±0.2)比假手术组:(2.2±0.1)pmol/(min.μg)](P<0.05);辛伐他汀能减轻心衰心肌的CaMKⅡ蛋白表达(1.2±0.1比心衰组:1.5±0.1)及活性[(2.8±0.1)比心衰组(3.5±0.2)pmol/(min.μg)](P<0.05)。结论辛伐他汀长期预防心力衰竭,能够改善心脏舒缩功能,可能与其降低CaMKⅡ蛋白表达及活性有关。
Background Heart failure (heart failure) is the ultimate result of various heart diseases caused by different causes. At present, there are still no reports on the changes of cardiac calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) and long-term intervention of simvastatin And then prevent heart failure reports. Objective To investigate the changes of myocardial CaMK Ⅱ protein expression and activity in rabbits with heart failure and the significance of long-term intervention of simvastatin. Methods Eighteen rabbits were randomly divided into three groups: sham-operation group, heart failure group and simvastatin group [10mg / (kg · d)], 6 rats in each group. Rabbits with heart failure The changes of left ventricular structure, hemodynamics and CaMKⅡexpression and activity were observed 7 weeks after operation. Results Left ventricular mass index (LVMI) was increased in CHF group (1.3 ± 0.1 vs 3.6 ± 0.1 g / kg vs LVEDD [sham operation group ± 1.8) than those in heart failure group (21.4 ± 2.5) mm], LVPW increased [sham operation group (2.0 ± 0.2) vs HF group (2.9 ± 0.8) mm], left ventricular end diastolic pressure (LVEDP) increased in the sham operation group (-1.5 ± 0.5 vs 23.0 ± 2.4 mmHg] (P <0.05); decreased left ventricular ejection fraction (LVFS) in the HF group [sham operation group (37.8 ± 3.6 ) (%, P <0.05). The left ventricular ejection fraction (LVEF) decreased in the sham-operated group (71.9 ± 4.6% vs 38.5 ± 6.1% Simvastatin could reduce LVMI [(2.1 ± 0.1) vs heart failure (3.6 ± 0.1) g / kg], LVEDD [(17.6 ± 1.9) vs 21.4 ± 2.5 mm], LVPW [(2.1 ± (P <0.05), LVEDP [(33.8 ± 2.5)%) was significantly higher than that of heart failure group (2.9 ± 0.8) mm] and LVEDP [(2.2 ± 0.8) vs 23.0 ± 2.4 mmHg] (17.4 ± 3.1)%] and LVEF [(63.2 ± 3.5)% vs 38.5 ± 6.1% (P <0.05) respectively). The CaMKⅡprotein expression in heart failure group was significantly higher than that in sham operation group (1.5 ± 0.1 vs 0.9 ± 0.1 vs sham operation group: (3.5 ± 0.2) vs. (2.2 ± 0.1) pmol / (min.μg) 0.05). Simvastatin could decrease the expression of CaMKⅡ in heart failure (1.2 ± 0.1 vs 1.5 ± 0.1) and activity [(2.8 ± 0.1) vs 3.5 ± 0.2 pmol / (min. μg)] (P <0.05). Conclusion Long-term prevention of heart failure by simvastatin can improve cardiac systolic and diastolic function, which may be related to the decrease of CaMKⅡ protein expression and activity.