Oxypurinol inhibits free radical release from the cerebral cortex of closed head injured rats.
Traumatic brain injury (TBI) is a significant cause of mortality and morbidity. Although the sequence of events underlying the resultant neuronal loss is still poorly understood, there are indications that oxygen-free radical generation is critically involved. Free radical generation in the cerebral cortex of closed head injury rats was monitored by measuring free radical release into cortical superfusates containing the spin trap agent 4-pyridyl-1-oxide-N-tert-butylnitrone (POBN, 100 mM). ESR analysis of the superfusates revealed six line spectra (alpha N = 15.4 G and alpha H beta = 2.5 G) characteristic of POBN-OH adducts. Administration of oxypurinol (40 mg/kg) 15 min prior to TBI prevented the formation of these radical adducts.
Sen
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Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Goldman
H
H
Morehead
M
M
Murphy
S
S
Phillis
J W
JW
D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D006259:Craniocerebral Trauma / Q000378:metabolism*; D004569:Electroencephalography / Q000187:drug effects; D004578:Electron Spin Resonance Spectroscopy; D005609:Free Radicals / Q000378:metabolism*; D009589:Nitrogen Oxides; D010117:Oxypurinol / Q000494:pharmacology*; D011725:Pyridines; D051381:Rats; D013113:Spin Labels
D005609:Free Radicals; D009589:Nitrogen Oxides; D011725:Pyridines; D013113:Spin Labels; C043438:alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone; D010117:Oxypurinol