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作 者:陈霞[1] 李英骥[2] 葛静岩[2] 张文杰[2] 钟国赣[2]
机构地区:[1]吉林大学基础医学院药理学教研室,吉林长春130021 [2]吉林大学基础医学院生理学教研室,吉林长春130021
出 处:《吉林大学学报(医学版)》2004年第5期704-706,共3页Journal of Jilin University:Medicine Edition
基 金:吉林省科技厅资助课题 (2 0 0 30 4 30 )
摘 要:目的 :观察氧化苦参碱 (OMT)对正常及乌头碱诱发大鼠心律失常模型动作电位 (AP)的影响。方法 :采用悬浮微电极技术记录大鼠在体心室肌细胞的动作电位。结果 :给予 3、 15和 30 m g· kg- 1 的 OMT能剂量依赖性地延缓乌头碱所致大鼠心律失常的发生 ,静脉给予 30 m g· kg- 1 的 OMT能减小 AP的幅值 ,缩短 APD50 和APD90 ,降低 Vmax。结论 :OMT对心肌细胞 AP的影响可能为其抗心律失常作用机制之一。Objective To observe the effects of oxymatrine on action potential in normal rats and arrhythmic rats induced by aconitine. Methods Action potential of ventricular myocytes of rats were recorded by suspended electrods. Results The oxymatrie at different doses(5,15, and 30 mg·kg -1 ) could delay the onset time of the arrhythmia induced by aconitine in dose-dependent manner in rats. After intravenous adminstration of oxymatrine(30 mg·kg -1 ) ,the average amplitude of the action potentials was reduced; the action potentials duration, measured at the 50% and 90% repolarization levels, was shortened; and maximum upstroke velocity of action potential was significantly decreased. Conclusion These results suggest that oxymatrine may inhibit cardiac sodium current.
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