Acute effects of amiodarone on sodium currents in isolated neonatal ventricular myocytes: comparison with procainamide.

F Chen, G T Wetzel, T S Klitzner
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引用次数: 10

Abstract

Recent studies suggest that amiodarone's acute clinical effects in infants and children are related predominantly to its class I antiarrhythmic activity. However, the effects of amiodarone on Na+ currents have not been investigated directly in immature cardiac cells. Accordingly, the tight seal whole cell voltage clamp technique was used to measure time- and voltage-dependent Na+ currents in acutely isolated neonatal ventricular myocytes from 2- to 5-day-old rabbits, before and after addition of amiodarone (0.1-10 microM). To evaluate the class I antiarrhythmic activity of amiodarone in this age group, the effects of amiodarone on Na+ currents were compared with those of procainamide. Similar to procainamide, amiodarone significantly decreased peak inward Na+ current in neonatal ventricular myocytes. Moreover, both amiodarone and procainamide shifted the steady-state inactivation curve to more negative membrane potentials and delayed recovery of the Na+ current from inactivation. Thus, the effects of amiodarone on the Na+ current in immature myocardium are qualitatively similar to those of procainamide, suggesting that amiodarone may act acutely as a class I antiarrhythmic agent in the newborn heart.

胺碘酮对分离新生儿心室肌细胞钠电流的急性影响:与普鲁卡因胺的比较。
最近的研究表明,胺碘酮在婴儿和儿童中的急性临床作用主要与其I类抗心律失常活性有关。然而,胺碘酮对Na+电流的影响尚未在未成熟心脏细胞中直接研究。因此,我们采用全细胞紧封电压钳技术,在添加胺碘酮(0.1-10微米)前后,测量2 ~ 5日龄家兔急性分离新生儿心室肌细胞的时间和电压依赖性Na+电流。为了评价胺碘酮在该年龄组的I类抗心律失常活性,我们比较了胺碘酮与普鲁卡因胺对Na+电流的影响。与普鲁卡因胺类似,胺碘酮显著降低新生儿心室肌细胞内Na+电流峰值。此外,胺碘酮和普鲁卡因胺均使稳态失活曲线向更负的膜电位偏移,并延迟Na+电流从失活中恢复。因此,胺碘酮对未成熟心肌Na+电流的影响在性质上与普鲁卡因胺相似,提示胺碘酮可能在新生儿心脏中作为I类抗心律失常药物发挥急性作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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