alpha-(4-pyridyl-1-oxide)-n-tert-butylnitrone has been researched along with Brain-Ischemia* in 2 studies
2 other study(ies) available for alpha-(4-pyridyl-1-oxide)-n-tert-butylnitrone and Brain-Ischemia
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Amflutizole, a xanthine oxidase inhibitor, inhibits free radical generation in the ischemic/reperfused rat cerebral cortex.
Free radical generation and release from the cerebral hemispheres of rats subjected to four-vessel occlusion elicited cerebral ischemia/reperfusion was monitored using a cortical cup technique with the spin-trapping agent alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN). Electron spin resonance (ESR) was used to detect the presence of free radical adducts of POBN in the cortical superfusates. Thirty min of ischemia plus reperfusion resulted in the release of .OH radical adducts during ischemia and especially in the initial stages of reperfusion. Pretreatment with the xanthine oxidase inhibitor, amflutizole (30 mg/kg) virtually abolished free radical formation and release. These results are consistent with earlier evidence that xanthine oxidase activity contributes to free radical formation in the ischemic/reperfused rat brain. Topics: Animals; Blood Pressure; Brain Ischemia; Cerebral Cortex; Electroencephalography; Electron Spin Resonance Spectroscopy; Free Radicals; Male; Nitrogen Oxides; Pyridines; Rats; Rats, Sprague-Dawley; Reperfusion; Spin Labels; Thiazoles; Xanthine Oxidase | 1994 |
Detection of free radicals during brain ischemia and reperfusion by spin trapping and microdialysis.
Extracellular free radicals were detected in rat striatal perfusate samples by intracerebral microdialysis coupled to the spin trapping technique. Five Sprague-Dawley rats were subjected to 30 min of global ischemia followed by reperfusion; throughout the experimental period the intrastriatal dialysing probe was perfused with Ringer's solution containing the spin trap agent pyridyl-N-oxide-t-butylnitrone (100 mM) together with the iron chelating agent diethylentriaminepentacetic acid (100 microM). A radical adduct occurred during ischemia and early reperfusion, but not in basal conditions; the spin adduct was characterized as a carbon centered radical, consistent with the presence of an oxidative attack on membrane lipids. The direct evidence of the formation of free radicals supports the hypothesis that free radicals play a role in the pathogenesis of the histological damage during brain ischemia. Topics: Animals; Brain Ischemia; Cyclic N-Oxides; Dialysis; Free Radicals; Nitrogen Oxides; Pyridines; Rats; Rats, Inbred Strains; Reperfusion; Spin Labels; Thiobarbiturates | 1992 |