Revenko S V, Khodorov B I, Avrutskiĭ M Ia
Biull Eksp Biol Med. 1980 Jun;89(6):702-4.
The blocking action of the antiarrhythmic cordaron (amiodaron hydrochloride) on Na currents in the frog node of Ranvier was studied by the voltage-clamp technique. It was established that the degree of the cordaron-induced block can be reversibly increased by long-term (1 s and more) membrane depolarization. The time constants of both the development and recovery from the block caused by membrane depolarization are of the order of hundreds of seconds ("induced slow sodium inactivation"). The fraction of blocked channels rises to some limiting level with an increase in the magnitude of the depolarizing step, the region of strong voltage dependency being between -130 and -70 mv. The inhibition of outward potassium current by 7.10(-4) M cordaron does not exceed 15%. The time- and voltage-dependent block of Na channels is supposed to result from interaction of the antiarrhythmic with inactivated channels.
采用电压钳技术研究了抗心律失常药物可达龙(盐酸胺碘酮)对青蛙郎飞结处钠电流的阻断作用。结果表明,长期(1秒及以上)的膜去极化可使可达龙诱导的阻断程度可逆性增加。由膜去极化引起的阻断发展和恢复的时间常数均在数百秒量级(“诱导性慢钠失活”)。随着去极化步幅大小的增加,被阻断通道的比例上升至某一极限水平,强电压依赖性区域在-130至-70毫伏之间。7.10(-4)M可达龙对外向钾电流的抑制不超过15%。钠通道的时间和电压依赖性阻断被认为是该抗心律失常药物与失活通道相互作用的结果。