O'Regan M H, Smith-Barbour M, Perkins L M, Cao X, Phillis J W
Department of Physiology, School of Medicine, Wayne State University, Detroit, MI 48201.
Neuropharmacology. 1994 Oct;33(10):1197-201. doi: 10.1016/s0028-3908(05)80010-3.
The efflux of hypoxanthine, xanthine and uric acid into cortical superfusates was studied with the cortical cup technique in the rat. Twenty minutes of four vessel occlusion followed by reperfusion results in a massive increase in the efflux of these purine metabolites. Amflutizole, 10 microM administered topically into the cortical cups, enhanced the ischemia-evoked release of hypoxanthine while it suppressed xanthine formation. Uric acid levels were not affected. Amflutizole also eliminated the ischemia/reperfusion-evoked generation of free radical adducts of alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN) detected by electron spin resonance. These results are consistent with a block of xanthine oxidase by amflutizole and support the involvement of xanthine oxidase in free radical mediated tissue damage following ischemia/reperfusion.
采用皮质杯技术在大鼠中研究了次黄嘌呤、黄嘌呤和尿酸向皮质灌流液中的外流量。四血管闭塞20分钟后再灌注会导致这些嘌呤代谢产物的外流量大幅增加。将10微摩尔的氨氟替唑局部注入皮质杯，可增强缺血诱发的次黄嘌呤释放，同时抑制黄嘌呤的形成。尿酸水平不受影响。氨氟替唑还消除了通过电子自旋共振检测到的缺血/再灌注诱发的α-(4-吡啶基-1-氧化物)-N-叔丁基亚硝基苯(POBN)自由基加合物的生成。这些结果与氨氟替唑对黄嘌呤氧化酶的阻断作用一致，并支持黄嘌呤氧化酶参与缺血/再灌注后自由基介导的组织损伤。
