Toyama J, Furuta T
Jpn Circ J. 1983 Jan;47(1):82-91. doi: 10.1253/jcj.47.82.
For the purpose to evaluate the effects of lidocaine on the ventricular arrhythmias occurring as complications of acute myocardial ischemia or infarction, the electrophysiological actions of lidocaine were estimated, as compared with those of procainamide, on the right ventricular papillary muscle of the rabbit heart superfused with hypoxic, hyperkalemic and/or acidic Krebs-Ringer solution. Lidocaine (1 to 5 x 10(-5)M) and procainamide (1.7 to 3.4 x 10(-5)M) depressed the maximum rate of action potential upstroke (Vmax) and prolonged both of the effective refractory period (ERP) and the diastolic interval needed for the premature Vmax to recover to 98% in magnitude of the basic Vmax (98% recovery time) dose-dependently, without decreasing the resting potential. Among the ischemic components, low pH (pH 6.9) and high potassium (10 mM) extracellular environments potentiated the depressant actions of lidocaine in synergic manner, but no significant enhancement of the actions of procainamide were observed under exposure to any components of ischemia. Mechanisms underlying the difference of the depressant actions on ischemic myocardium between lidocaine and procainamide were discussed in the light of recent concepts of actions of local anesthetics, and came to the conclusion that lidocaine is the most preferable antiarrhythmic agent for the management of ventricular arrhythmias during acute ischemia or infarction.
为了评估利多卡因对急性心肌缺血或梗死并发症所发生的室性心律失常的影响，在灌注缺氧、高钾和/或酸性 Krebs-Ringer 溶液的兔心脏右心室乳头肌上，将利多卡因的电生理作用与普鲁卡因胺的电生理作用进行比较，从而对利多卡因的电生理作用进行评估。利多卡因（1至5×10⁻⁵M）和普鲁卡因胺（1.7至3.4×10⁻⁵M）剂量依赖性地降低动作电位最大上升速率（Vmax），并延长有效不应期（ERP）和使早搏Vmax恢复到基础Vmax幅度的98%所需的舒张间期（98%恢复时间），而不降低静息电位。在缺血成分中，低pH（pH 6.9）和高钾（10 mM）细胞外环境以协同方式增强利多卡因的抑制作用，但在暴露于任何缺血成分时，未观察到普鲁卡因胺作用的显著增强。根据局部麻醉药作用的最新概念，讨论了利多卡因和普鲁卡因胺对缺血心肌抑制作用差异的潜在机制，并得出结论，利多卡因是治疗急性缺血或梗死期间室性心律失常的最优选抗心律失常药物。
