Protection of the ischemic myocardium calcium-free cardioplegic infusates and the additive effects of coronary infusion and ischemia in the induction of the calcium paradox.
Studies in the globally ischemic, isolated rat heart have shown that the preischemic coronary infusion of calcium-free cardioplegic solution may lead to an exacerbation of the postischemic leakage of creatine kinase. This exacerbation could be prevented by the inclusion of trace amounts of calcium in the coronary infusate or could be postponed by the omission of calcium during postischemic reperfusion. The calcium paradox, observed with such a combination of coronary infusion and ischemia required for its induction a less extensive cellular calcium depletion than that induced by infusion only and was the result of 2 additive factors: the washout of tissue calcium during preischemic infusion and the cellular influx of residual membrane-bound calcium during ischemia. The balance between protective and damaging properties with calcium-free cardioplegic infusates was influenced by the concentration of Na+, K+, Mg++ and procaine in the infusates as these agents influence patterns of calcium redistribution.
D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology*; D002462:Cell Membrane / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D006324:Heart Arrest, Induced / Q000379:methods*; D066298:In Vitro Techniques; D008274:Magnesium / Q000494:pharmacology; D009206:Myocardium / Q000378:metabolism; D009994:Osmolar Concentration; D010477:Perfusion; D011343:Procaine / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000494:pharmacology; D012996:Solutions
D012996:Solutions; D011343:Procaine; D012964:Sodium; D003402:Creatine Kinase; D008274:Magnesium; D002118:Calcium