Malécot C, Coraboeuf E, Coulombe A
Am J Physiol. 1984 Sep;247(3 Pt 2):H429-39. doi: 10.1152/ajpheart.1984.247.3.H429.
The effects of low concentrations of Ba have been studied on dog Purkinje fibers and on guinea pig left ventricular epicardium. In both tissues, Ba induces diastolic depolarization at a membrane potential more negative than -80 mV. This effect becomes clearly detectable at concentrations as low as 10-20 microM in Purkinje fibers bathed in 5.4 mM K Tyrode solution and around 100 microM in ventricular epicardium. In both tissues the Ba-induced depolarization is blocked in a dose-dependent manner by low concentrations of Cs (0.5-5 mM) as is the normal pacemaker current (if) in Purkinje fibers. In ventricular muscle the Ba-induced depolarization develops at the same rate whether the tissue is at rest or depolarized by repetitive stimulation. The maximum (initial) slope of diastolic depolarization is insensitive to D 600, La, and 4-aminopyridine, increased by tetraethylammonium chloride, decreased by tetrodotoxin, and almost entirely suppressed by Na removal. Experimental data and reconstruction of electrical activity suggest that in ventricular muscle the Ba-induced diastolic depolarization results to a large extent from the unmasking of a small pacemaker inward current, mainly carried by Na ions and similar to the pacemaker current of Purkinje fibers. Unmasking of the depolarizing effect of the pacemaker current is very likely due to the decrease by Ba of the inward going rectification. Steady-state inward Na current flowing through the Na window can increase the diastolic depolarization. Residual Cs-insensitive, Ba-induced diastolic depolarization may result from a time-dependent blockade of the background K conductance like the one described in skeletal muscle.
低浓度钡对犬浦肯野纤维和豚鼠左心室心外膜的影响已得到研究。在这两种组织中，钡在膜电位比 -80 mV 更负时诱导舒张期去极化。在 5.4 mM K 台氏液中浸泡的浦肯野纤维中，低至 10 - 20 μM 的浓度时这种效应就可明显检测到，而在心室心外膜中约为 100 μM 时可明显检测到。在这两种组织中，低浓度的铯（0.5 - 5 mM）以剂量依赖的方式阻断钡诱导的去极化，就像浦肯野纤维中的正常起搏电流（if）一样。在心室肌中，无论组织处于静息状态还是通过重复刺激去极化，钡诱导的去极化以相同的速率发展。舒张期去极化的最大（初始）斜率对 D 600、镧和 4 - 氨基吡啶不敏感，被氯化四乙铵增加，被河豚毒素降低，并且几乎完全被去除钠离子所抑制。实验数据和电活动重建表明，在心室肌中，钡诱导的舒张期去极化在很大程度上是由于一种小的起搏内向电流的暴露，该电流主要由钠离子携带，类似于浦肯野纤维的起搏电流。起搏电流去极化作用的暴露很可能是由于钡使内向整流减少所致。流经钠通道窗口的稳态内向钠电流可增加舒张期去极化。残留的对铯不敏感的钡诱导的舒张期去极化可能是由于背景钾电导的时间依赖性阻断，就像在骨骼肌中所描述的那样。
