Evidence That Free Radicals Result in Reperfusion Injury in Heart Muscle

Abstract

Recently, with the advent of thrombolytic therapy and emergency angioplasty for acute infarction interest in reperfusion injury has intensified. The question is whether all myocardial necrosis is reflective of the duration and severity of ischemia or whether there are cells which are alive at the end of the period of ischemia and undergo necrosis as a result of events that occur during or after reperfusion. These comments are entirely limited to three specific issues free-radical- induced reperfusion injury. Our group came into this area of free radical injury to heart muscle subsequent to the early studies of Drs. McCord¹, Luchessi² and Hearse³ and their colleagues. Therefore, we had the opportunity to focus our attention to three specific issues that we viewed as pivotal: (1) Are mechanisms that have been proposed to produce free radicals at the moment of reperfusion supported by direct measured oxygen based free radicals? (2) Does superoxide dismutase (SOD) administered as a therapeutic agent into the perfusate have any directly measurable effect on the presumed burst of oxygen free radicals on reperfusion. There has been considerable doubt as to whether SOD in the perfusate can reduce injurious, possibly intracellularly generated radicals?