Chikharev V N, Mal'tsev V A, Rozenshtraukh L V
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR. 1981;4(2):58-66.
The effect of lidocaine on the transmembrane ion currents of normal and partially depolarized atrial trabecula was studied in the frog by fixation of membrane potential with duoble sucrose bridge. Lidocaine in a concentration below 12 X 10(-4) g/ml produced no effect on the slow input current. Lidocaine decreased the potassium conduction at the membrane potential values below--45 mW, and increased at--30 mW. Kinetic parameters of the rapid input sodium current and its amplitude significantly changed under the action of lidocaine in normal cardiac tissue, and its effect increased in the depolarized tissue. It is suggested that depolarization is a factor increasing sensitivity to lidocaine of rapid sodium canals, while the capacity of lidocaine to inhibit effectively the rapid sodium current in the partially depolarized myocardium determine its antiarrhythmic activity.
采用双蔗糖桥固定膜电位的方法,在青蛙身上研究了利多卡因对正常和部分去极化心房小梁跨膜离子电流的影响。浓度低于12×10⁻⁴ g/ml的利多卡因对慢内向电流无影响。在膜电位低于 -45 mV时,利多卡因降低钾离子传导;在 -30 mV时,利多卡因增加钾离子传导。在正常心脏组织中,利多卡因作用下快速内向钠电流的动力学参数及其幅度发生显著变化,在去极化组织中其作用增强。提示去极化是增加快速钠通道对利多卡因敏感性的一个因素,而利多卡因有效抑制部分去极化心肌快速钠电流的能力决定了其抗心律失常活性。