Satoh H, Hashimoto K
Jpn J Pharmacol. 1986 Jan;40(1):83-93. doi: 10.1254/jjp.40.83.
Effects of procaine (50-500 micrograms/ml) on membrane potential and currents were investigated using a two microelectrode-voltage clamp technique. Procaine reduced the action potential amplitude (APA), the maximum diastolic potential and the maximum rate of depolarization (Vmax) in a dose-dependent manner. At the same time, the action potential duration and the cycle length were prolonged. In voltage clamp experiments, procaine (50 micrograms/ml) did not affect the slow inward current (Isi), but reduced the time-dependent outward current (Ik). At concentrations higher than 100 micrograms/ml, procaine reduced both currents and the inward current activated by hyperpolarization in a dose-dependent manner. In 7 of 20 specimens, a low concentration of procaine (50 or 100 micrograms/ml) increased Isi which enhanced the Vmax and APA, but did not increase Ik. Procaine did not affect the steady-state inactivation of Isi (f infinity) and the activation of Ik (p infinity). The results suggest that the depressions of currents induced by procaine are due to a reduction in conductances of the current systems.
采用双微电极电压钳技术研究了普鲁卡因(50 - 500微克/毫升)对膜电位和电流的影响。普鲁卡因以剂量依赖性方式降低动作电位幅度(APA)、最大舒张电位和最大去极化速率(Vmax)。同时,动作电位持续时间和周期长度延长。在电压钳实验中,普鲁卡因(50微克/毫升)不影响慢内向电流(Isi),但降低时间依赖性外向电流(Ik)。在浓度高于100微克/毫升时,普鲁卡因以剂量依赖性方式降低两种电流以及超极化激活的内向电流。在20个标本中的7个中,低浓度的普鲁卡因(50或100微克/毫升)增加了Isi,这增强了Vmax和APA,但未增加Ik。普鲁卡因不影响Isi的稳态失活(f无穷大)和Ik的激活(p无穷大)。结果表明,普鲁卡因诱导的电流降低是由于电流系统电导的降低。