Myocardial cation contents during induction of calcium paradox.
Myocardial cation contents were measured in isolated rat hearts perfused under various conditions. Reperfusion of Ca2+-deprived hearts produced marked increases in myocardial Ca2+ and Na+ and decreases in Mg2+ and K+ contents. These changes were dependent on the Ca2+ concentration and duration of perfusion during the periods of Ca2+ deprivation and reperfusion. The loss of Ca2+ and K+ contents normally seen after Ca2+-free exposure as well as the reperfusion-induced changes were prevented if the Ca2+-free medium contained low (35 mM) Na+ or was cooled to 21 degrees C. Reperfusion with normal Ca2+, low Na+ medium augmented the increase in myocardial Ca2+ content, while reducing K+ or Mg2+ or increasing Mg2+ in the reperfusion medium had no effect. Addition of verapamil, D600, or propranolol to the reperfusion solution did not alter the reperfusion-induced cation changes observed using control medium. These data suggest that during Ca2+ depletion, the mechanisms responsible for regulating calcium influx are either lost or inactivated, so that reperfusion-induced changes are governed solely by the driving force favoring calcium influx. The occurrence of Ca2+ overload under this condition has been implicated in the irreversible damage to myocardium and contractile failure.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D066298:In Vitro Techniques; D007700:Kinetics; D008274:Magnesium / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D014700:Verapamil / Q000494:pharmacology
D012964:Sodium; D011433:Propranolol; D014700:Verapamil; D008274:Magnesium; D011188:Potassium; D002118:Calcium