Reoxygenation injury in the heart, also known as the “oxygen paradox”, is characterized by the sudden release of cytoplasmic constituents upon reoxygenation of the myocardium following a sustained period of hypoxia. In recent years, reactive oxygen species have been indirectly implicated in producing cardiac reoxygenation injury in some model systems through the protection provided by various antioxidants (Ambrosio et al., 1987; Granger et al., 1986; Hess and Manson, 1984). However, other studies have failed to find such protection (Gallagher et al., 1986; Klein et al., 1988; Nejima et al., 1989; Uraizee et al., 1987) and our results (Kehrer et al., 1987), and those of other investigators (Bindoli et al., 1988; Vander Heide et al., 1987), indicated extracellular oxygen radicals are not involved in the oxygen paradox. Nevertheless, a variety of electron spin resonance studies have indicated that oxygen radicals are produced at reoxygenation (Arroyo et al., 1987; Baker et al., 1988; Garlick et al., 1987; Zweier, 1988). The production of free radicals during the ischemic period has also been reported (Baker and Kalyanaraman, 1989; Maupoil and Rochette, 1988; Rao et al., 1983). The unanswered question is whether any of these radicals, which may be generated intracellularly, are actually interacting with various tissue components to produce damage.