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Herz 1997 Jun;22 Suppl 1:35-9


Effect of magnesium on infarct size after coronary occlusion. Animal experiment studies


[Article in German]


Thamer V, Grunert S, Bier F, Schlack W.

Institut fur Herz- und Kreislaufphysiologie, Heinrich-Heine-Universitat, Dusseldorf.


In addition to its antiarrhythmic and antithrombotic effects magnesium is said to have a beneficial effect in patients with acute myocardial infarction. Magnesium can protect myocardial tissue after coronary occlusion and reduces infarct size in experimental models of ischaemia and reperfusion, though the given doses of magnesium are relatively high and differ from clinically reachable serum concentrations.


We tested 2 hypotheses in a dog model of ischaemia-reperfusion:


1. The protective effect may be due to a direct, local influence of magnesium on myocardial reperfusion injury.

2. Systemic magnesium treatment with low doses comparable to clinical study regiments may reduce myocardial infarct size.


Anaesthetized open chest dogs underwent 1 h of left anterior descending artery occlusion followed by 6 h of reperfusion.


1. Ten animals received intracoronary magnesium aspartate (Mg i.c.) or vehicle infusion (control i.c.) for the first hour of reperfusion to increase regional Mg-concentration by 2 mmol/l.

2. Fourteen animals received intravenous infusion with magnesium potassium aspartate (Mg-K i.v.) or vehicle infusion (control i.v.), beginning 1 h before occlusion until the end of the 6 h reperfusion period.


Regional magnesium concentration in the Mg i.c.-group increased to 2.7 +/- 1.00 mmol/l at 45 min of reperfusion. Intravenous infusion raised serum magnesium from 0.71 +/- 0.03 mmol/l to 1.29 +/- 0.14 mmol/l in the Mg-K i.v. group (5 min of reperfusion, p < 0.01 vs. baseline).


Infract size after 6 h reperfusion (TTC staining) was similar in both groups of intracoronary treatment (Mg i.c., 20.6 +/- 5.0; control, 24.4 +/- 8.7% of area at risk; p = n.s.) and intravenous treatment (Mg-K i.v. 18.1 +/- 14.8; control 14.1 +/- 12.2% of area at risk; p = n.s.).


Neither regional nor systemic magnesium leads to a clinically relevant reduction of infarct size in the regional ischaemic-reperfused dog heart when it is given in clinically usable doses.


The beneficial action of systemic Mg is probably not due to an early direct protective effect on ischaemic-reperfused myocardium but to its antiarrhythmic and antithrombotic effects. Possibly only to high doses of Mg applied under experimental conditions can reduce infarct size.




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