李泱, 牛慧燕, 刘念, 张存泰, 陆再英, 王士雯. 长期应用咪达普利对陈旧性心肌梗死代偿区不应期和钠电流的影响J. 药学学报, 2005, 40(7): 654-658.
引用本文: 李泱, 牛慧燕, 刘念, 张存泰, 陆再英, 王士雯. 长期应用咪达普利对陈旧性心肌梗死代偿区不应期和钠电流的影响J. 药学学报, 2005, 40(7): 654-658.
LI Yang, NIU Hui-yan, LIU Nian, ZHANG Cun-tai, LU Zai-ying, WANG Shi-wen. Effect of imidapril on the effective refractory period and sodium current of ventricular noninfarction zone in healed myocardial infarctionJ. Acta Pharmaceutica Sinica, 2005, 40(7): 654-658.
Citation: LI Yang, NIU Hui-yan, LIU Nian, ZHANG Cun-tai, LU Zai-ying, WANG Shi-wen. Effect of imidapril on the effective refractory period and sodium current of ventricular noninfarction zone in healed myocardial infarctionJ. Acta Pharmaceutica Sinica, 2005, 40(7): 654-658.

长期应用咪达普利对陈旧性心肌梗死代偿区不应期和钠电流的影响

Effect of imidapril on the effective refractory period and sodium current of ventricular noninfarction zone in healed myocardial infarction

  • 摘要: 目的探讨咪达普利(IMI)对家兔陈旧性心梗(HMI)后心脏有效不应期(ERP)及钠电流(INa)的影响。方法选家兔制HMI模型,口服IMI 0.625 mg·kg-1·d-1(8周)。记录整体心脏ERP和单细胞INa。结果HMI组ERP显著延长,用IMI后则缩短。HMI组代偿区细胞INa降低,INa稳态失活曲线负移,恢复时间常数延长;应用IMI,INa明显恢复。结论咪达普利可抑制HMI心脏ERP延长,并使降INa得以恢复。这可能是该药减少陈旧性心梗后心律失常发生的机制之一。

     

    Abstract: AimTo investigate the effects of imidapril (IMI) on effective refractory period (ERP) and sodium current (INa) of myocytes in ventricular noninfarction zone of healed myocardial infarction (HMI) in rabbit models. MethodsRabbits with left coronary artery ligation were prepared and IMI (0625 mg·kg-1·d-1, 8 weeks) was orally administered. The ERP and sodium current were recorded. ResultsThe ERP in HMI heart was prolonged. The ERP in IMI group was lower significantly than that of HMI group. The INa density of myocyte in HMI ventricle decreased obviously. V1/2 of steady state inactivation of INa shifted to hyperpolarization, and time constant (τ) of recovery from inactivation in HMI ventricular myocyte was longer than that of sham ventricular myocyte. INa density in IMI group increased markedly as compared with that of HMI group. ConclusionIMI was shown to reverse the abnormal prolongation of ERP in rabbit heart with the HMI and increase INa density. It may be the mechanism of IMI preventing against antiarrhythmia in healed myocardical infarction.

     

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