The monovalent reduction of oxygen yields two reduced intermediate forms: the dioxide anion (O2), hydrogen peroxide H2O2, and the hydroxyl radical (OH.) several of which appear as radicals. Under normal conditions, the concentration of free oxygen radicals in the tissues is closely controlled because of the serious cell lesions which an accumulation of these radicals can cause. The aim of this paper was to discuss the origin and role of free oxygen radicals in cell lesions induced by myocardial ischemia/perfusion as well as results obtained in different experimental models using methods to trap these radicals. Overall these experimental results are encouraging and appear to offer new therapeutic possibilities which, however, have been evaluated only barely in man.