Chapman R A, Fozzard H A, Friedlander I R, January C T
Am J Physiol. 1986 Dec;251(6 Pt 1):C920-7. doi: 10.1152/ajpcell.1986.251.6.C920.
Sheep cardiac Purkinje fibers were exposed to solutions free of divalent cations for hour-long periods, while intracellular Na+ and K+ activities were measured using ion-sensitive microelectrodes. Intracellular Na+ activity (aiNa) increased to 50.1 +/- 8.1 mM, and intracellular K+ activity (aiK) decreased to 76.7 +/- 3.5 mM. These ionic changes could be blocked by the presence of Mg2+ or the Ca2+ channel blocking agents D 600 and nifedipine. The rise in aiNa and the fall in aiK was accentuated by the inhibition of the Na+-K+ pump with acetylstrophanthidin or by removal of extracellular K+. These results demonstrate that in cardiac Purkinje fibers removal of divalent cations produces intracellular loading of Na+ by Na+ entry through the Ca2+ channel. On reexposure to Ca2+-containing solutions, the cells become loaded with Ca2+, and the fibers exhibit large contractures. These observations implicate Na+-Ca2+ exchange in the entry of Ca2+ into these cells during Ca2+ repletion and in the etiology of the calcium paradox.
将绵羊心脏浦肯野纤维暴露于无二价阳离子的溶液中长达一小时,同时使用离子敏感微电极测量细胞内Na⁺和K⁺活性。细胞内Na⁺活性(aiNa)增加到50.1±8.1 mM,细胞内K⁺活性(aiK)降低到76.7±3.5 mM。这些离子变化可被Mg²⁺的存在或Ca²⁺通道阻滞剂D 600和硝苯地平阻断。用乙酰毒毛旋花子苷抑制Na⁺-K⁺泵或去除细胞外K⁺会加剧aiNa的升高和aiK的降低。这些结果表明,在心脏浦肯野纤维中,去除二价阳离子会通过Na⁺经Ca²⁺通道进入细胞而导致细胞内Na⁺负荷增加。当重新暴露于含Ca²⁺的溶液中时,细胞会被Ca²⁺负荷,并且纤维会出现大的挛缩。这些观察结果表明,Na⁺-Ca²⁺交换参与了Ca²⁺再充盈期间Ca²⁺进入这些细胞的过程以及钙反常的病因学。