Alabovskiĭ V V, Vinokurov A A
Biokhimiia. 1992 Oct;57(10):1540-7.
Increasing of extracellular sodium concentration up to 200 mM diminishes heart damage under "calcium paradox". Phosphocreatine (10(-4) M) potentiates the effect of high sodium perfusion media; in this case myoglobin release from the myocardium is minimal (5-9% of control). An the same time, ATP and phosphocreatine concentrations and oxidation to phosphorylation coupling in mitochondria remain at a sufficiently high level. Elevation of osmotic pressure by the effect of 120 mM sucrose enhances heart damage under "calcium paradox" both in the presence and absence of phosphocreatine. The protective effects of superhigh (200 mM) sodium concentrations and phosphocreatine are completely reversed by strophanthin or decreasing K+ concentration down to 0.5 mM.
将细胞外钠浓度提高到200 mM可减轻“钙反常”情况下的心脏损伤。磷酸肌酸（10⁻⁴ M）可增强高钠灌注培养基的作用；在这种情况下，心肌中肌红蛋白的释放最少（为对照的5 - 9%）。同时，三磷酸腺苷（ATP）和磷酸肌酸的浓度以及线粒体中的氧化磷酸化偶联仍保持在足够高的水平。在有和没有磷酸肌酸的情况下，120 mM蔗糖的作用引起的渗透压升高都会增强“钙反常”情况下的心脏损伤。毒毛花苷或将钾离子浓度降至0.5 mM可完全逆转超高（200 mM）钠浓度和磷酸肌酸的保护作用。
