[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.
Wang
X W
XW
Department of Pharmacology, Xinjiang Medical College, Urumqi, China.
Zhang
J L
JL
Zhou
C M
CM
Wang
X F
XF
Liu
W J
WJ
Zhang
K J
KJ
D000818:Animals; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D007545:Isoproterenol; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D017202:Myocardial Ischemia / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000201:enzymology; D010672:Phenytoin / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism
D008315:Malondialdehyde; D010672:Phenytoin; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D007545:Isoproterenol