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目的研究哇巴因对大鼠心肌重构的作用。方法雄性Sprague-Dawly(SD)大鼠22只随机分为哇巴因组(n=12)及对照组(n=10),经腹腔注射哇巴因[20μg/(kg·d)]和生理盐水[1mL/(kg·d)]8周构建动物模型。第6周,根据收缩压情况,将哇巴因组分为哇巴因敏感鼠(收缩压升高,n=10)和哇巴因抵抗鼠(收缩压没有明显升高,n=2)。电镜下观察3组心肌的超微结构变化,同时实时定量PCR检测其电压门控性K+通道4.2(Kv4.2)表达水平的变化;通过膜片钳方法研究哇巴因对大鼠心室肌细胞动作电位及瞬间外向钾电流(Ito)的影响。结果从第6周起,与对照组比较,10只哇巴因敏感鼠收缩压明显升高[(138.2±8.0)比(120.1±5.2)mmHg,P<0.01];2只哇巴因抵抗鼠收缩压无明显变化[(126.7±11.4)比(125.4±6.9)mmHg,P>0.05]。哇巴因敏感鼠电镜观察其左心室心尖部中层心肌组织可见线粒体肿胀等超微结构改变。哇巴因抵抗鼠心肌细胞超微结构较对照组差异无统计学意义。RT-PCR提示3组大鼠心肌Kv4.2表达差异无统计学意义。膜片钳结果提示哇巴因敏感鼠心室肌细胞动作电位时程延长,Ito密度下调,引起心肌电重构。结论哇巴因引起大鼠血压升高的同时引起心肌结构重构及电重构。
Objective To investigate the effect of ouabain on cardiac remodeling in rats. Methods Twenty-two male Sprague-Dawly rats were randomly divided into ouabain group (n = 12) and control group (n = 10), intraperitoneal injection of ouabain (20μg / (kg · d) Saline [1 mL / (kg · d)] for 8 weeks. At Week 6, ouabain was classified into ouabain-sensitive rats (systolic blood pressure increase, n = 10) and ouabain-resistant rats (systolic blood pressure did not rise significantly, n = 2) according to systolic blood pressure. The ultrastructural changes of myocardium were observed under electron microscope. The changes of voltage-gated K + channel 4.2 (Kv4.2) expression were detected by real-time quantitative polymerase chain reaction. The effects of ouabain on ventricular myocytes Action potential and transient outward potassium current (Ito). Results Compared with the control group, the systolic blood pressure of 10 ouabain-sensitive rats increased significantly from the 6th week ([(138.2 ± 8.0) vs (120.1 ± 5.2) mmHg, P <0.01] There was no significant change in systolic BP [(126.7 ± 11.4) vs. (125.4 ± 6.9) mmHg, P> 0.05]. Ouabain sensitive mouse electron microscopy of the left atrial apical central myocardial tissue visible mitochondrial swelling and other ultrastructural changes. The ultrastructure of ouabain-resistant rat cardiac myocytes was not significantly different from the control group. RT-PCR suggested that there was no significant difference in Kv4.2 expression between the three groups. Patch clamp results suggest that ouabain sensitive ventricular myocytes prolonged action potential duration, Ito density decreased, causing cardiac electrical remodeling. Conclusion ouabain induced cardiac hypertrophy and electrical remodeling in rats.