Sestoft L, Folke M
Department of Medicine F, Gentofte Hospital, Hellerup, Denmark.
Am J Physiol. 1990 Jan;258(1 Pt 1):G45-51. doi: 10.1152/ajpgi.1990.258.1.G45.
The effects of low flow and reestablished normal flow on K+ balance and carboxylic acid balance was studied in perfused liver of 48-h starved rats at perfusate pH 7.4 and 6.8. The rate of net K+ release induced by ouabain was 1.8 mumol.min-1.g-1 at pH 7.4 and 1.4 mumol.min-1.g-1 at pH 6.8. Lowering of flow to 30% normal was accompanied by a transient, diphasic loss of K+ (max 0.15 mumol.min-1.g-1). Reestablished normal flow was immediately accompanied by a monophasic K+ uptake (max 0.35 mumol.min-1.g-1). These changes in potassium balance were independent of perfusate pH. Reduction of flow caused an almost immediate depolarization of 4 mV followed by a steady tendency to repolarization. Reestablished normal flow induced a transient hyperpolarization. Production of carboxylic acids during the low flow period did not correlate with the diphasic time course of K+ loss, and carboxylic acid uptake after reestablishment of flow did not correlate with the transient uptake of K+. The data show that the initial phase of K+ loss during low flow is due to inhibition of the Na(+)-K(+)-pump; the second phase may be reasonably explained by increased K+ permeability concomitant to cellular volume regulation.
在灌注液pH值为7.4和6.8的条件下，研究了低流量和恢复正常流量对48小时饥饿大鼠灌注肝脏中钾离子平衡和羧酸平衡的影响。在pH值为7.4时，哇巴因诱导的钾离子净释放速率为1.8 μmol·min⁻¹·g⁻¹，在pH值为6.8时为1.4 μmol·min⁻¹·g⁻¹。将流量降至正常流量的30%会伴随着钾离子的短暂双相性丢失（最大值为0.15 μmol·min⁻¹·g⁻¹）。恢复正常流量后立即伴随着单相性钾离子摄取（最大值为0.35 μmol·min⁻¹·g⁻¹）。钾离子平衡的这些变化与灌注液pH值无关。流量降低几乎立即导致4 mV的去极化，随后有稳定的复极化趋势。恢复正常流量会诱导短暂的超极化。低流量期间羧酸的产生与钾离子丢失的双相时间进程不相关，流量恢复后羧酸的摄取与钾离子的短暂摄取也不相关。数据表明，低流量期间钾离子丢失的初始阶段是由于钠钾泵受到抑制；第二阶段可以合理地解释为与细胞体积调节相关的钾离子通透性增加。
