Ren Yanping, Zhang Mingjuan, Zhang Ting, Huang Ruowen
Geriatric-Cardiovascular Department, The First Affiliated Hospital, Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061;
Exp Ther Med. 2013 Jul;6(1):65-70. doi: 10.3892/etm.2013.1098. Epub 2013 May 2.
The aim of this study was to investigate the effect of ouabain (EO) on myocardial remodeling. Twenty-two adult male Sprague-Dawley rats were randomly divided into two groups: the rats in the EO group (n=12) were intraperitoneally injected with EO daily and those in the control group (n=10) were injected with physiological saline daily. After 8 weeks the rats were sacrificed. The ultrastructural changes in the myocardium were observed. The expression levels of voltage-gated potassium channel 4.2 (K4.2) were detected by real-time quantitative reverse transcription-polymerase chain reaction. The effects of EO on the myocardial action potential and transient potassium efflux (I) were measured by patch clamping. The systolic blood pressure (SBP) of 10 of the 12 rats in the EO group, designated as the EO-sensitive (OS) rats, began to increase from the fifth week of treatment and was significantly higher compared with that of the control group 6 weeks later (P<0.01). The remaining 2 rats in the EO group that presented no increase in SBP following 8 weeks of treatment (P>0.05) were designated as EO-resistant (OR) rats. Pathological ultrastructural changes were significant in the apical mid-myocardium of the OS rats. No significant differences in K4.2 expression were observed among the OS, OR and control rats. The patch clamp results revealed that EO prolongs the action potential duration, reduces I and triggers the electrical remodeling of the myocardium. EO induces a blood pressure increase and triggers structural and electrical remodeling.
本研究旨在探讨哇巴因（EO）对心肌重塑的影响。将22只成年雄性Sprague-Dawley大鼠随机分为两组：EO组（n = 12）大鼠每天腹腔注射EO，对照组（n = 10）大鼠每天注射生理盐水。8周后处死大鼠，观察心肌超微结构变化，采用实时定量逆转录-聚合酶链反应检测电压门控钾通道4.2（K4.2）的表达水平，通过膜片钳检测EO对心肌动作电位和瞬时钾外流（I）的影响。EO组12只大鼠中有10只的收缩压（SBP）从治疗第5周开始升高，6周后与对照组相比显著升高（P<0.01），这10只大鼠被指定为EO敏感（OS）大鼠。EO组其余2只大鼠在治疗8周后SBP未升高（P>0.05），被指定为EO抵抗（OR）大鼠。OS大鼠心尖中层心肌的病理超微结构变化显著。OS、OR和对照组大鼠之间K4.2表达未观察到显著差异。膜片钳结果显示，EO延长动作电位时程，降低I并引发心肌电重塑。EO导致血压升高并引发结构和电重塑。
