摘要
目的探讨家兔慢性心力衰竭（心衰）时心肌钙调蛋白依赖性蛋白激酶Ⅱ（CaMKⅡ）蛋白表达及活性改变的意义。方法14只家兔随机分为2组，假手术组和心衰组各7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。结果与假手术组比，心衰组左心室重量指数[（1．3±0．1）g／kg比3．6±0．1）g／kg]、左室舒张末径[（13．3±1．8）him比（21．4±2．5）mm]、左室后壁厚度[（2．0±0．2）mm比（2．9±0．8）min]、左心室舒张末压[（01．5±O．5）mm Hg比（23．0±2．4）mmHg]明显升高（P〈0．05），左心室缩短率[（37．8±3．6）％比（17．4±3．1）％]及左室射血分数[（71．9±4．6）％比（38．5±6．1）％]明显降低（P〈O．05）；CaMKII蛋白表达（1．45±0．13）及活性[（3．54±0．17）pmol·min-1·μg-1]显著高于假手术组[（O．89±0．05），（2．18±0．13）pmol·min-1·μg-1]（P〈0．05）。结论心肌CaMKⅡ蛋白表达及活性增加可能是导致心力衰竭的发生因素之一。
Objective To investigate the expression and activity of Calcium/calmodulin-dependent pro- tein kinase- Ⅱ （CaMKⅡ ） in heart failure rabbit. Methods 14 rabbits were divided into two groups ： 6 rabbits with heart failure induced by volume overload plus pressure overload, 7 sham operated rabbits. 7 weeks later, left ven- tricular function, hemodynmnic parameters, expression and activity of CaMK Ⅱ were observed. Results Compared with the sham operated rabbits, LVMI [ （ 1.3 ±0.1 ）g/kg vs （ 3.6 ±0.1 ）g/kg ], LVEDD [ （ 13.3 ± 1.8 ）ram vs （ 21.4 ± 2.5）mm], LVPW [（2.0±0.2）mm vs （2.9±0.8）mm and LVEDP [（-1.5±0.5）mm Hg vs （23.0±2.4）mm Hg] in heart failure rabbits were significantly increased（P〈0.05）, but their left ventricular shorten fraction [ （37.8±3.6）% vs （17.4±3.1）% ] and ejection fraction [（71.9±4.6）% vs （38.5±6.1）% ] were decreased（P〈0.05）. Expression （1.45±0.13 vs 0.89±0.05） and activity[（3.54±0.17）pmol·min-1·μg-1 vs （2.18±0.13）pmol·min-1·μg-1] of CaMK 11 in heart failure rabbits were remarkably higher than sham operated rabbits （P〈0.05）. Conclusion Upregulation of expression and activity of CaMK Ⅱ might contribute to risk factors of dysfunction in failing hearts.
出处
《中国心血管病研究》
CAS
2010年第2期141-144,共4页
Chinese Journal of Cardiovascular Research
