Volume 2 Supplement 1

18th International Symposium on Intensive Care and Emergency Medicine

Open Access

Intravenous magnesium reduces infarct size following an ischaemia/reperfusion injury combined with a thrombogenic lesion in the LAD

  • HB Ravn1,
  • LB Ilkjaer1,
  • U Moeldrup1,
  • L Jensen1,
  • M Chew1,
  • S Johnsen1,
  • L Birk-Soerensen1,
  • E Tønnesen1 and
  • VE Hjortdal1
Critical Care19982(Suppl 1):P054

DOI: 10.1186/cc184

Published: 1 March 1998

Introduction

Experimental studies have demonstrated that magnesium (Mg) therapy can protect the ischemic myocardium and modulate reperfusion injury. In myocardial infarction the reperfusion injury is further complicated by the presence of a thrombogenic area in the affected coronary artery that may lead to repetitive reocclusion and embolisation.

Methods

We investigated the effect of Mg on infarct size in a randomised, blinded study in pigs inflicted with a thrombogenic lesion in the left anterior descending artery (LAD) and mechanical occlusion of the vessel proximal to the lesion. Coronary occlusion was maintained for 50 min followed by 4 h reperfusion. Magnesium sulphate (6 mmol/30 min followed by 3 mmol/h) or saline was given at 20 min of coronary occlusion and continued for 4 h. 111Indium-labeled platelets were given 30 min prior to harvesting of the hearts. Troponin-T (TNT) was measured at base-line and 3 h into reperfusion.

Results

The infarct size/area at risk (IS/AR) ratio in the placebo group was 40 (35–63)% (n = 8) compared with 16 (9–40)% (n = 6) in the Mg treated animals (P < 0.05). Platelet accumulation in AR was reduced with 15% in the Mg treated animals [placebo-group: 194 (157–205)% vs Mg-group: 166(131–213)%; NS]. Cellular leakage of TNT increased significantly in both groups and was at 3 h highest in the placebo group: 1.7 (0.6–3.5 μg/l compared to 0.3 (0.1–1.5) μg/l in the Mg-treated animals (NS).

Conclusion

The present study demonstrates that iv Mg infusion is able to reduce infarct size with more than 50% in this model where an ischaemia/reperfusion injury was combined with endothelial damage in the nutrient artery. The reduction in infarct size may be due to complementary actions on platelets and a cellular protection of the myocardium.

Authors’ Affiliations

(1)
Aarhus University Hospital

Copyright

© Current Science Ltd 1998

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