Anti-lipid peroxidation and protective effects of phenytoin sodium on ischemic myocardium of mice

Isoproterenol (Iso, 20 mg.kg-1 x d-1 x 2 d) induced widespread and severe myocardial damages at ultrastructural level, decreased the myocardial Se-glutathione peroxidase (Se-GSH-Px) and superoxide dismutase (SOD) activities, increased the serum creatine phosphokinase (CPK) concentration and myocardial malondialdehyde (MDA) content. Phenytoin sodium (Phe) 15 or 30 mg.kg-1 ip pretreatment diminished the CPK release and MDA production, protected the Se-GSH-Px activity in the Iso-induced damage of mouse heart. The pretreatment with 30 mg.kg-1 abated the reduction of SOD activity. However, Phe 15 mg.kg-1 did not show such an effect. Phe (15 or 30 mg.kg-1) reduced the ultrastructural cardiotoxicity of Iso, and the membrane structure of ischemic myocardium was protected. The protective effects of verapamil pretreatment 3 mg.kg-1 ip were weaker than those of Phe on ultrastructural changes, but biochemical changes were similar to those of Phe. The results suggested that Phe possessed anti-lipid peroxidation and protective effects on ischemic myocardium.