There is compelling, although indirect, evidence that oxygen free radi
cals, generated during ischemia as well as upon reperfusion and reoxyg
enation of the ischemic heart, contribute to the reversible ventricula
r dysfunction characterized as myocardial stunning. Evidence of cell m
embrane damage as well as depression of sarcoplasmic reticulum and mit
ochondrial function with resulting calcium overload of the cell may be
a result of lipid peroxidation of the cell by free radical products.
Radical scavenger enzymes have been shown to greatly reduce the appear
ance of mRNA of a stress response protein (heat shock protein 71) in a
pig heart model of stunning. The potential role for the introduction
of antioxidant enzymes or stress protein in the cell is presented as a
possible strategy for attenuating free radical damage during postisch
emic reflow.