[Significance of extracellular concentration of sodium ions in the protective effect during the "calcium paradox"].
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.
Alabovskiĭ
V V
VV
Vinokurov
A A
AA
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002414:Cations, Monovalent; D006321:Heart / Q000187:drug effects; D008929:Mitochondria, Heart / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D010085:Oxidative Phosphorylation; D010725:Phosphocreatine / Q000502:physiology*; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D013328:Strophanthins / Q000494:pharmacology
D002414:Cations, Monovalent; D013328:Strophanthins; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D012964:Sodium; D002118:Calcium
Znachenie vnekletochnoĭ kontsentratsii ionov natriia v osushestvlenii fosfokreatinom zashchitnogo deĭstviia pri "kal'tsevom paradokse".