The link between free radicals and myocardial injury

In the first part of this study, oxygen derived radicals (O2-radical) were indirectly demonstrated as causative agents for ischemia/reperfusion injury by showing myocardial protection of radical scavengers. In 19 open chest dogs, the left anterior descending coronary artery was occluded for 90 min and subsequently reperfused for 60 min. Group A received SOD (15000 U/kg), catalase (5 mg/kg) and 20% mannitol (18 ml/kg) via the left atrium starting 15 min pre-occlusion and ending 15 min after reperfusion. Group B received infusion of saline and served as control. The severity of myocardial injury was evaluated by epicardial ECG, hemodynamics, echo cardiographical asynergy area and left ventricular wall thickness, histopathological findings and magnitude of necrotic area. Group A demonstrated less injury than group B in most of the parameters. In particular, ratios of necrotic to perfused areas determined by dual fluorescence methods were significantly limited in group A (34.1 +/- 12.0 vs 66.0 +/- 11.3%), indirectly verifying that the O2- radicals play an important role in the genesis of ischema/reperfusion injury. In the second part of the study, the direct measurement of radicals in freeze-clamped myocardium was reported using electron spin resonance (ESR) spectroscopy. With this method, it was not possible to demonstrate the generation of O2-radicals in ischemic/reperfused myocardium. However, the data suggested that coenzyme Q10 anion radical, which exists in the normal myocardium, might provide an index of tissue injury.