Myocardial reoxygenation damage. Can it be circumvented?
Isolated papillary-muscle preparations from the cat and rabbit were used to study the phenomenon of reoxygenation contracture and whether is is amenable to intervention independently of the preceding hypoxic insult. Reduction of extracellular Ca2+ to "0" mM abolished reoxygenation contracture, but subsequent replacement of Ca2+ resulted in severe contracture and death due to the "calcium paradox." Lowering of Ca2+ to 0.125 mM and its stepwise replacement to 2.5 mM resulted in no contracture with good mechanical recovery. Gradual reoxygenation, Mg2+ (30 mM), Mn2+ (8 mM), or H+ (pH 6.5) ions, or diltiazem (10(-4) M) delayed but did not prevent the development of contracture and contractile failure. Unlike diltiazem, verapamil (10(-4) M) and lidoflazine (2 X 10(-5) M) did not significantly affect the contracture.
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002415:Cats; D003326:Coronary Circulation / Q000187:drug effects*; D004110:Diltiazem / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006863:Hydrogen-Ion Concentration; D008013:Lidoflazine / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D008345:Manganese / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects*; D010210:Papillary Muscles / Q000187:drug effects*; D011817:Rabbits; D014700:Verapamil / Q000494:pharmacology
D008345:Manganese; D014700:Verapamil; D004110:Diltiazem; D008274:Magnesium; D008013:Lidoflazine; D002118:Calcium