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  • Title: Hydroxyl radical generation after the third hour following ischemia contributes to brain damage.
    Author: Takamatsu H, Kondo K, Ikeda Y, Umemura K.
    Journal: Eur J Pharmacol; 1998 Jul 10; 352(2-3):165-9. PubMed ID: 9716351.
    Abstract:
    The purpose of the present study was to determine after what time period hydroxyl radical formation contributes most to ischemic brain damage in focal ischemia, using a hydroxyl radical scavenger, EPC-K1, L-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyl-tridecyl)-2H-1-be nzopyran-6yl-hydrogen phosphate] potassium salt. Focal ischemia was produced by thrombotic occlusion of the left middle cerebral artery in rats. After evaluation of the pharmacokinetics of EPC-K in the brain tissue and plasma following 10 mg/kg intravenous bolus treatment of conscious rats, we investigated the neuroprotective effect of EPC-K1 in the middle cerebral artery occlusion model. A single intravenous bolus of EPC-K1 was given immediately, 3 or 6 h after ischemia, and cerebral brain damage was measured 24 h after ischemia. When EPC-K1 was injected 3 h after ischemia, a significant (P < 0.01) reduction of cerebral brain damage was observed. EPC-K1 delivered by intravenous infusion that started immediately after ischemia and lasted for 24 h, also significantly (P < 0.05) reduced brain damage, but the efficacy of the neuroprotective effect was the same as that of the 3 h after ischemia bolus treatment. These results may indicate that the period of hydroxyl radical formation most critical for ischemic brain damage is a few hours after the third hour following ischemia in this model.
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