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Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:569-574

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:569-574.)
© 1999 American Heart Association, Inc.


Original Contributions

Intravenous Magnesium Reduces Infarct Size After Ischemia/Reperfusion Injury Combined with a Thrombogenic Lesion in the Left Anterior Descending Artery

Hanne B. Ravn; Ulla Moeldrup; Carl I. O. Brookes; Lars B. Ilkjaer; Paul White; Michelle Chew; Liselotte Jensen; Soeren Johnsen; Lene Birk-Soerensen; Vibeke E. Hjortdal

From the Institute of Experimental and Clinical Research (H.B.R., U.M., M.C., S.J., L.B.-S.), Aarhus University, and the Department of Anaesthesiology (H.B.R., M.C., L.J.), the Department of Cardiology (U.M.), and the Department of Thoracic and Cardiovascular Surgery (L.B.I., V.E.H.) Aarhus University Hospital, Aarhus, Denmark; and the Department of Cardiology (C.I.O.B, P.W.), Royal Brompton Hospital, London, UK.

Correspondence to Hanne B. Ravn, MD, PhD, Institute of Experimental and Clinical Research, Skejby Hospital, DK-8200 Aarhus N, Denmark. E-mail hbr{at}iekf.aau.dk

Abstract—Experimental studies have demonstrated that intravenous magnesium (Mg) can protect the ischemic myocardium and has an antithrombotic effect. In patients with myocardial infarction, the reperfusion injury is complicated by the presence of a thrombogenic area in the affected coronary artery that may cause repetitive thrombus formation and embolization. We investigated the effect of Mg on infarct size in a randomized study in pigs. Myocardial infarction was induced by a 50-minute mechanical occlusion of the left anterior descending artery combined with an arterial injury, which stimulated a dynamic thrombus formation with emboli shedding on reperfusion. Magnesium sulfate (6 mmol/20 min plus 3 mmol/h) or saline was started at 30 minutes after coronary occlusion. Real-time ventricular pressure–volume loops were generated from the left ventricle by using a microtip pressure manometer and a conductance catheter. Platelet accumulation in the myocardium was evaluated by using 111In-labeled platelets. After 4 hours of reperfusion, the infarct size/area at risk ratio in the placebo group was 46±0.06% (n=8) compared with 22±0.07% (n=6) in the Mg-treated animals (P=0.03). Ejection fraction decreased significantly in the control group but not in the Mg-treated animals (P=0.03). Platelet accumulation in the myocardium did not change significantly between the Mg- and placebo-treated animals (placebo group, 191±19%; Mg group, 177±29%; NS). The present study demonstrates that intravenous Mg infusion is able to reduce infarct size by >50% and preserve the ejection fraction in this model where ischemia/reperfusion injury was evaluated in the presence of a thrombogenic area in the nutrient artery.


Key Words: magnesium • animals • reperfusion injury • thrombosis • platelets




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