Khuri R N, Agulian S K, Abdulnour-Nakhoul S, Nakhoul N L
Department of Medicine, School of Medicine, East Carolina University, Greenville, North Carolina 27858-4354.
J Cell Physiol. 1992 Dec;153(3):534-8. doi: 10.1002/jcp.1041530314.
Intracellular potassium and membrane potential were measured simultaneously by means of double-barrelled liquid ion-exchange microelectrodes in single fibers of rat thigh muscle in vivo in rats maintained in seven different metabolic states. The K+ equilibrium potential (EK) was more negative than the simultaneously measured membrane potential (Em) in the normal state by 18.4 mV. K+ loading, acute and chronic, resulted in depolarization of Em due to increased serum K+ (hyperkalemia) with no increase in intracellular K+. K+ depletion resulted in hyperpolarization of Em as plasma K+ decreased proportionately more than intracellular K+. Low Na+ diet had no effect. Intracellular K+ was decreased in acute acidosis but not in the chronic state. Thus K+ depletion and acute acidosis are associated with intracellular K+ decrease. The fact that hyperpolarization exists in the former and not the latter is a reflection that hypokalemia accompanies the former condition. The hyperpolarizing states of K+ depletion and chronic acidosis are accompanied by decreased excitability and muscle weakness.
在处于七种不同代谢状态的大鼠体内,通过双管液体离子交换微电极同时测量大鼠大腿肌肉单纤维中的细胞内钾和膜电位。在正常状态下,钾离子平衡电位(EK)比同时测量的膜电位(Em)负18.4 mV。急性和慢性钾负荷导致Em去极化,原因是血清钾升高(高钾血症),而细胞内钾没有增加。钾缺乏导致Em超极化,因为血浆钾下降的比例比细胞内钾下降的比例更大。低钠饮食没有影响。急性酸中毒时细胞内钾减少,但慢性状态下则不然。因此,钾缺乏和急性酸中毒与细胞内钾减少有关。前者存在超极化而后者不存在这一事实反映出低钾血症伴随前者情况。钾缺乏和慢性酸中毒的超极化状态伴随着兴奋性降低和肌肉无力。