Free radical production is enhanced in both the ischemic core and penumbral following stroke injury, and this is believed to cause much of the damage seen in the core as well as penumbra. There are many agents that either block free radical production or inhibit its activation that have been shown to be very effective in experimental models. Uric acid is a well-known natural antioxidant present in fluids and tissues. Administration of uric acid resulted in a highly significant reduction in ischemic damage and improved behavioral outcome (Yu et al., 1998). Edaravone, Tetramethylpyrazine, alpha-phenyl-N-tert-butyl-nitrone, FR210575, and NXY-59 are other free radical inhibitors that were effective against experimental stroke injury. EGb-761 is a free radical scavenger derived from a concentrated extract of Ginkgo that is currently in a phase 2 clinical trial (Legos et al., 2002). Clinical trials with free radical scavengers have had limited success after acute ischemic stroke, but have had more success in the treatment of subarachnoid hemorrhage. Patients administered nicaraven after subarachnoid hemorrhage had a reduced rate of delayed ischemic neurologic deficits. NXY-59 was well tolerated in patients with stroke and currently is being studied for efficacy by AstraZeneca Pharmaceuticals.
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