The role of the neutrophil and free radicals in ischemic myocardial injury

Abstract

The association of coronary artery thrombosis with the onset of acute myocardial infarction has provided the rationale for the development of pharmacologic and/or physical methods for the restoration of coronary artery blood flow. The institution of pharmacologic methods for myocardial reperfusion has resulted in a reduction in mortality leading to acceptance of thrombolytic therapy as the standard approach to the management of patients with an evolving acute myocardial infarction [I]. It is a well established fact that prolonged myocardial ischemia leads to a time-dependent loss in the viability of myocardial cells in the jeopardized region of the heart and that the restoration of coronary artery blood flow is fundamental in order to arrest the progression of cell death and for the restoration of myocardial function. The restoration of blood flow is essential for repair of the reversible changes induced by ischemia and for the continued survival of the myocardial cells at risk of permanent damage. The reintroduction of oxygen at the time of reperfusion, however, may be detrimental to the reoxygenated myocyte as well as being beneficial. A number of recent reviews have been devoted to an examination of the question of whether reactive species of oxygen or oxygen radicals can contribute to the development of irreversible myocardial cell injury during the period of reperfusion [2, 3, 4, 51. The purpose of this editorial is to focus attention on the potential role of the polymorphonuclear leukocyte (PMN) as a determinant of the ultimate extent of irreversible myocardial injury after ischemia and reperfusion, and to call attention to those factors which modulate the inflammatory response to myocardial cell injury.