Phillis J W, Sen S
Department of Physiology, Wayne State University, Detroit, MI 48201.
Brain Res. 1993 Nov 19;628(1-2):309-12. doi: 10.1016/0006-8993(93)90970-x.
Free radical generation and release from the cerebral hemispheres of rats subjected to four vessel occlusion followed by reperfusion was monitored using a cortical cup technique in conjunction 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. 30 min of ischemia plus reperfusion resulted in the release of .OH radical adducts during the period of ischemia and, especially, during the initial phases of reperfusion. No radical adducts were detectable 90 min after the onset of reperfusion. Pretreatment with the xanthine oxidase inhibitor, oxypurinol (40 mg/kg i.p.), virtually abolished free radical formation and release. The results of this study are consistent with earlier evidence of free radical formation during ischemia/reperfusion and suggest that the cerebroprotective actions of oxypurinol may be related to its ability to prevent the cascade of free radical generation.
采用皮质杯技术结合自旋捕获剂α-（4-吡啶基-1-氧化物）-N-叔丁基硝酮（POBN），监测四动脉闭塞再灌注大鼠大脑半球自由基的产生和释放。利用电子自旋共振（ESR）检测皮质灌流液中POBN的自由基加合物。30分钟的缺血加再灌注导致在缺血期间，特别是在再灌注初期释放出·OH自由基加合物。再灌注开始90分钟后未检测到自由基加合物。用黄嘌呤氧化酶抑制剂氧嘌呤醇（40mg/kg腹腔注射）预处理，几乎完全消除了自由基的形成和释放。本研究结果与早期关于缺血/再灌注期间自由基形成的证据一致，并表明氧嘌呤醇的脑保护作用可能与其预防自由基生成级联反应的能力有关。
