Elharrar V, Bailey J C, Lathrop D A, Zipes D P
J Pharmacol Exp Ther. 1978 May;205(2):410-7.
The electrophysiologic effects of aprindine hydrochloride were studied on normal Purkinje fibers, on Purkinje fibers superfused with Tyrode's solution containing 22 mM KCl and isoproterenol (1 X 10(-5) M) and on transient depolarizations induced by exposure to acetylstrophanthidin (1.7--2 X 10(-7) M). Aprindine (3 X 10(-6) M) significantly reduces the action potential amplitude and dV/dtmax and shortens the action potential duration but does not alter the resting membrane potential. Transient depolarizations were suppressed by aprindine at a dose of 2 X 10(-6) M. Isoproterenol (1 X 10(-5) M) failed to restore the transient depolarizations after suppression with aprindine. Slow responses induced in K-depolarized, isoproterenol-treated fibers were unchanged by aprindine (3 X 10(-6)-1 X 10(-5) M) in the presence as well as in the absence of acetylstrophanthidin. These experiments suggest that aprindine does not have slow channel blocking properties and that an inward current through the slow channel cannot be considered as the sole basis of the digitalis-induced transient depolarization.
研究了盐酸阿普林定对正常浦肯野纤维、用含22 mM氯化钾和异丙肾上腺素(1×10⁻⁵ M)的台氏液灌流的浦肯野纤维以及暴露于毒毛花苷(1.7 - 2×10⁻⁷ M)诱导的瞬时去极化的电生理效应。阿普林定(3×10⁻⁶ M)显著降低动作电位幅度和最大dV/dt,并缩短动作电位持续时间,但不改变静息膜电位。阿普林定在剂量为2×10⁻⁶ M时可抑制瞬时去极化。异丙肾上腺素(1×10⁻⁵ M)在用阿普林定抑制后未能恢复瞬时去极化。在钾去极化、异丙肾上腺素处理的纤维中诱导的慢反应,无论有无毒毛花苷,阿普林定(3×10⁻⁶ - 1×10⁻⁵ M)均未使其改变。这些实验表明,阿普林定不具有慢通道阻断特性,并且通过慢通道的内向电流不能被视为洋地黄诱导的瞬时去极化的唯一基础。