Summary
To determine the effect of magnesium on myocardial function and oxidative metabolism after reperfusion, isolated rat hearts perfused retrogradely with erythrocyte-enriched medium (0.4 mM palmitate bound to 0.4 mM albumin, 11 mM glucose) were subjected to 60 minutes of no-flow ischemia followed by 60 minutes of reperfusion. Untreated postischemic hearts exhibited after 15 minutes of reperfusion recovery of myocardial oxygen consumption to 65% of the preischemic value despite persistent depression of left ventricular isovolumic pressure development to 21%. Magnesium (15 mM) administered during the initial 30 minutes of reperfusion reduced myocardial oxygen consumption of reperfuse myocardium by 35%. Oxidation of [1-14C]palmitate was slightly more reduced (−55%) than oxidation of [U-14C]glucose(−42%). Magnesium did not influence ultimate recovery of contractile function and cumulative myocardial release of creatine kinase. Thus, 15 mM magnesium administered during reperfusion elicited a reduction of oxidative metabolism. However, magnesium did not modify myocardial injury.
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Supported by the Swiss National Science Foundation grant 32-26373.89 and the Swiss Foundation of Cardiology
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Tamm, C., Papageorgiou, I., Tardy, I. et al. Effect of magnesium administered during postischemic reperfusion on myocardial oxidative metabolism in isolated rat hearts. Basic Res Cardiol 89, 366–379 (1994). https://doi.org/10.1007/BF00795204
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DOI: https://doi.org/10.1007/BF00795204