Objective: The purpose of this study was to elucidate a role for edaravone, a free radical scavenger 3-methyl-1-phenyl-2-pyrazolin-5-one, in neonatal hypoxic-ischemic brain damage. We determined the level of thiobarbituric acid reactive Substances as in index of lipid peroxidation and nitric oxide metabolites as nitric oxide production. Study design: Seven-day-old Wistar rats were subjected to left common carotid artery ligation followed by 2 hours of 8% oxygen exposure. Then, the rats were administered edaravone (9 mg/k) or saline solution intraperitoneally. Cerebrospinal fluid was withdrawn just before file rats 9 were killed at 2, 5 24, and 48 hours after hypoxia, and brains were removed. The thiobarbituric acid reactive Substances and nitric oxide metabolites levels were measured in the brain tissue and cerebrospinal fluid, respectively. Results: On the ligated side, edaravone significantly decreased thiobarbituric acid reactive Substances levels at 5 and 24 hours after hypoxia, compared with saline group (P < .01). Edaravone significantly decreased the nitric oxide metabolites level in the cerebrospinal fluid only at 5 hours, compared with saline group (P < .01). Conclusion: Edaravone potently and transiently inhibited lipid peroxidation and the production of nitric oxide in the neonatal rat brain after hypoxic-ischemic insult. (C) 2005 Mosby, Inc. All rights reserved.
