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Cardioprotective Effects of Mitochondrial-Targeted Antioxidants in Myocardial Ischemia/Reperfusion (I/R) Injury Reactive oxygen species (ROS) generated during myocardial I/R contribute to post-reperfused cardiac contractile dysfunction. Damaged cardiomyocyte mitochondria are major sites of excess ROS generation during reperfusion. We hypothesized that reducing mitochondrial ROS formation should attenuate myocardial I/R injury and thereby improve function of isolated perfused rat hearts subjected to I(30min)/R(45min) compared to untreated I/R hearts. Mitoquinone (MitoQ, MW=579g/mol; complexed with cyclodextrin (MW=1135g/mol) to improve water solubility, total MW=1714g/mol), a coenzyme Q derivative, and SS-31 (Szeto-Schiller) peptide ((D-Arg)-Dmt-LysPhe-Amide, MW=639g/mol, Genemed Synthesis, Inc., San Antonio, TX), an alternating cationic-aromatic peptide, are selective mitochondrial ROS inhibitors which significantly improved post-reperfused cardiac function compared to untreated I/R controls in this study (p<0.05). MitoQ elicits antioxidant effects through the recycling of ubiquinone to ubiquinol, whereas SS-31 utilizes an antioxidant dimethyltyrosine residue. Improvement in postreperfused cardiac function by MitoQ or SS-31 was associated with a significant decrease in myocardial tissue infarct size compared to untreated I/R hearts (p<0.01). These results suggest mitochondrial-derived ROS are important contributors to I/R injury, and MitoQ or SS-31 when administered at reperfusion may potentially augment the benefits of angioplasty or