EFFECTS OF LIGNOCAINE AND QUINIDINE ON THE PERSISTENT SODIUM CURRENT IN RAT VENTRICULAR MYOCYTES
EFFECTS OF LIGNOCAINE AND QUINIDINE ON THE PERSISTENT SODIUM CURRENT IN RAT VENTRICULAR MYOCYTES
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DOI：
10.1111/j.1476-5381.1992.tb12743.x
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发表时间：
1992-10-01
影响因子：
7.3
通讯作者：
GAGE, PW
中科院分区：
文献类型：
--
作者：
JU, YK;SAINT, DA;GAGE, PW
1 采用全细胞、紧密密封记录技术，在大鼠离体心室肌细胞中检查了 1 类抗心律失常药物利多卡因和奎尼丁对动作电位以及去极化激活的钠电流和钾电流的影响。2 河鲀毒素和利多卡因缩短了动作电位平台期的持续时间，而奎尼丁延长了动作电位平台期的持续时间。3 在低浓度下，利多卡因和奎尼丁阻断了持续的钠电流，而奎尼丁延长了动作电位平台期的持续时间。具有抗失活能力，但它们对瞬时钠电流的影响很小。在较高浓度下，它们还阻断瞬时钠电流。 4 奎尼丁（但不是河豚毒素或利多卡因）抑制了去极化激活的钾电流，这可能是奎尼丁引起的平台期延长的原因。 5 有人认为，持续钠电流的阻断可能是（至少部分）利多卡因和奎尼丁的抗心律失常作用的原因。
1 The effects of the Class 1 antiarrhythmic agents lignocaine and quinidine on action potentials, and on sodium currents and potassium currents activated by depolarization, were examined in rat isolated ventricular myocytes by the whole cell, tight seal recording technique.2 Tetrodotoxin and lignocaine shortened, whereas quinidine prolonged, the duration of the plateau phase of action potentials.3 At low concentrations, lignocaine and quinidine blocked a persistent sodium current that was resistant to inactivation but they had only a small effect on the transient sodium current. At higher concentrations, they also blocked the transient sodium current.4 Quinidine, but not tetrodotoxin or lignocaine, depressed potassium currents activated by depolarization and this could account for the prolongation of the plateau phase caused by quinidine.5 It is suggested that block of the persistent sodium current may be responsible, at least in part, for the antiarrhythmic action of lignocaine and quinidine.