Carmeliet E
Laboratory of Physiology, University of Leuven, Campus Gasthuisberg, Belgium.
Circ Res. 1988 Jul;63(1):50-60. doi: 10.1161/01.res.63.1.50.
The blocking mechanism of the Na+ channel by penticainide, a disopyramide analogue, was studied in rabbit cardiac Purkinje fibers. Na+ channel activity was measured directly by recording the slowly inactivating Na+ current or indirectly by measuring Vmax. The two-microelectrode technique was used to measure currents under voltage-clamp conditions or to impose different degrees and durations of depolarizing pulses. The experimental results show 1) that penticainide exerted a pronounced use-dependent block not dependent on the duration of the depolarizing pulse, 2) that no block was observed in the absence of stimulation, even when the membrane was depolarized by conditioning prepulses, and 3) that recovery was slower the more negative the holding potential but could be accelerated by repeating the depolarizing pulse; there was not only use-dependent block but also use-dependent unblock. It is concluded that penticainide binds to the open Na+ channel and is trapped when the activated channel returns to the rested state.
在兔心脏浦肯野纤维中研究了丙吡胺类似物喷替卡因对钠通道的阻滞机制。通过记录缓慢失活的钠电流直接测量钠通道活性,或通过测量Vmax间接测量。采用双微电极技术在电压钳制条件下测量电流,或施加不同程度和持续时间的去极化脉冲。实验结果表明:1)喷替卡因产生明显的使用依赖性阻滞,不依赖于去极化脉冲的持续时间;2)在无刺激时,即使通过预处理脉冲使膜去极化,也未观察到阻滞;3)静息电位越负,恢复越慢,但重复去极化脉冲可加速恢复;不仅存在使用依赖性阻滞,还存在使用依赖性解除阻滞。得出的结论是,喷替卡因与开放的钠通道结合,并在激活的通道恢复到静息状态时被捕获。