Alabovskiĭ V V, Vinokurov A A
Biokhimiia. 1992 Oct;57(10):1532-9.
Perfusion of isolated rat hearts with a phosphocreatine (10(-4) M) containing solution to which strophanthin or KCl had been added up to a concentration of 27 mM as well as Ca2+ depletion decreased phosphocreatine concentration in the perfusate with a simultaneous increase in creatine and phosphocreatine concentrations in the myocardium. Neither high extracellular concentrations of Na+ (200 mM), nor phosphocreatine increased creatine and phosphocreatine levels in the myocardium. The effect of high sodium perfusion media was completely reversed by strophanthin. Phosphocreatine decreased the lactate content in the perfusate. Strophanthin or potassium chloride enhanced the effect of phosphocreatine on the lactate release. Conversely, creatine augmented the lactate content in the perfusate. A high specificity of the phosphocreatine effect on the myocardium independently of the ionic composition of the perfusate was postulated. A mechanism of protective effects of phosphocreatine and high sodium perfusion media on "calcium paradox" is proposed.
用含有磷酸肌酸（10⁻⁴ M）的溶液灌注离体大鼠心脏，该溶液中加入了毒毛花苷或氯化钾，浓度高达27 mM，同时去除钙离子，这会降低灌注液中磷酸肌酸的浓度，同时心肌中肌酸和磷酸肌酸的浓度会增加。细胞外高浓度的钠离子（200 mM）和磷酸肌酸均不会增加心肌中肌酸和磷酸肌酸的水平。毒毛花苷可完全逆转高钠灌注培养基的作用。磷酸肌酸可降低灌注液中的乳酸含量。毒毛花苷或氯化钾增强了磷酸肌酸对乳酸释放的作用。相反，肌酸会增加灌注液中的乳酸含量。推测磷酸肌酸对心肌的作用具有高度特异性，与灌注液的离子组成无关。提出了磷酸肌酸和高钠灌注培养基对“钙反常”的保护作用机制。
