Abstract
The effects of oxygen-derived radical scavengers (ODRS) on the heart was investigated during the calcium paradox. Perfusion with Ca2 +-free medium caused cell separation at the intercalated discs and changes in the endothelial cells. Upon Ca2+ reintroduction, a massive cell damage occurred. The cytosolic enzyme, creatine phosphokinase (CPK), was released in large amounts (p< 0.001). The tissue adenosine triphosphate (ATP) was reduced to 3.7 μmol/g dry weight from the control value of 21.6 μmol/g dry weight and tissue Ca2+ content was increased threefold. The treatment with Superoxide dismutase (SOD) and catalase (CAT) increased percentage of normal cells (62.2%) compared to nontreated Ca2+ paradox group (0.2%) and caused negligible leakage of CPK. Tissue ATP was preserved (p2+ content was also reduced in the hearts treated with SOD and CAT (p2+ paradox injury.