Intracoronary and Intravenous Magnesium Does Not Reduce Myocardial Infarct Size in a Canine Model of Regional Ischaemia and Reperfusion

Journal of Clinical and Basic Cardiology 2002; 5 (1): 23-28

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Keywords: Herz,  Hund,  Infarktgröße,  Ischämie,  magnesium,  Myokardinfarkt,  reperfusion,  dog,  heart,  infarct size,  ischaemia,  magnesium,  myocardial infarction,  reperfusion

Clinical trials show controversial effects of magnesium infusion in patients with acute myocardial infarction. In LIMIT-2, intravenous magnesium lowered mortality, but in the much larger ISIS-4, intravenous magnesium had no effect. Because of these conflicting results, we tested two hypotheses in a dog model of ischaemia and reperfusion. A) Intracoronary magnesium infusion given in the early reperfusion period has a protective effect against myocardial reperfusion injury. B) Systemic magnesium-potassium infusion with doses comparable to those used in clinical studies, may reduce myocardial infarct size. Anaesthetized open chest dogs underwent 1 h of left anterior descending artery occlusion followed by 6 h of reperfusion. A) Animals received intracoronary magnesium aspartate (Mg i.c., n = 5) or vehicle infusion (Control i.c., n = 5) for the first hour of reperfusion to increase regional plasma concentration by 4 mmol l?1. B) Animals received intravenous magnesium-potassium-aspartate (Mg-K i.v., n = 6) or vehicle infusion (Control i.v., n = 8) beginning 1 h before occlusion until the end of the 6 h reperfusion period. Intracoronary magnesium had no influence on infarct size (Mg i.c. 20.6 ± 5.0 % of area at risk, Control i.c. 24.4 ± 8.7 % of area at risk, P = ns) or regional post-ischaemic wallfunction. Application of intravenous magnesium-potassium did not reduce myocardial infarct size (Mg-K i.v. 14.1 ± 14.8 %; Control i.v. 18.1 ± 12.2 % of area at risk; P = ns). The possible beneficial effect of magnesium infusion is probably not due to an early, direct protective effect on ischaemic-reperfused myocardium.