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British Medical Bulletin 43:460-471 (1987)
© 1987 The British Council

research-article

Inflammation and myocardial infarction

S W Werns and B R Lucchesi

Department of Internal Medicine (Division of Cardiology), The University of Michigan Medical School Ann Arbor, Michigan, USA
Department of Pharmacology, The University of Michigan Medical School Ann Arbor, Michigan, USA

Abstract

Myocardial ischemia causes the release of chemotactic factors, migration of neutrophils, peroxidation of lipids, and myocardial cellular depletion of free radical scavengers. The invading neutrophils may injure the myocardial vasculature and sarcolemma by generating oxygen free radicals. Several agents that affect neutrophils or oxygen radicals were evaluated in a canine model of regional myocardial ischemia and reperfusion. Anaesthetised dogs underwent occlusion and reperfusion of the left circumflex coronary artery. Limitation of infarct size by ibuprofen was associated with marked suppression of leukocyte accumulation within the ischemic myocardium. Neutrophil depletion by antiserum resulted in similar reductions in ultimate infarct size and was accompanied by a reduction in leukocyte infiltration. A combination of the oxygen radical scavenger superoxide dismutase plus the enzyme, catalase, decreased myocardial injury whether infusion began before occlusion or 75 minutes after occlusion. None of the treatments significantly altered haemodynamic indices of myocardial oxygen demand. Reduction of infarct size by ibuprofen, neutrophil antiserum, and free radical scavengers indicates that neutrophils and oxygen radicals participate in producing the irreversible damage to the myocardium during ischemia and reperfusion.


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