Phillis J W, Sen S, Cao X
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Neurosci Lett. 1994 Mar 14;169(1-2):188-90. doi: 10.1016/0304-3940(94)90388-3.
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.
采用带有自旋捕捉剂α-(4-吡啶基-1-氧化物)-N-叔丁基硝酮(POBN)的皮质杯技术，监测四动脉闭塞诱发脑缺血/再灌注的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缺血期间尤其是再灌注初始阶段·OH自由基加合物的释放。用黄嘌呤氧化酶抑制剂安氟唑(30mg/kg)预处理几乎完全消除了自由基的形成和释放。这些结果与早期证据一致，即黄嘌呤氧化酶活性促成缺血/再灌注大鼠脑内自由基的形成。
