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Abstract
Toxic oxygen metabolites (TOM) are generated by activated leukocytes and ischemic tissue upon reperfusion, and are cardiotoxic in vitro. Generation of TOM during reperfusion in vivo has been measured directly and indirectly. TOM contribute to myocardial stunning, causing systolic and diastolic dysfunction. TOM may also play a role in the pathogenesis of reperfusion arrhythmias. It is uncertain if TOM cause cell death during reperfusion. Inhibition of TOM with antioxidants may be important for myocardial protection during cardiac surgery.
