Zini I, Tomasi A, Grimaldi R, Vannini V, Agnati L F
Institute of Human Physiology, University of Modena, Italy.
Neurosci Lett. 1992 Apr 27;138(2):279-82. doi: 10.1016/0304-3940(92)90933-x.
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.
通过将脑内微透析与自旋捕获技术相结合，在大鼠纹状体灌流液样本中检测细胞外自由基。五只Sprague-Dawley大鼠经历30分钟的全脑缺血，随后再灌注；在整个实验期间，纹状体内透析探针用含有自旋捕获剂吡啶基-N-氧化物-叔丁基硝酮（100 mM）和铁螯合剂二乙三胺五乙酸（100 microM）的林格氏液灌注。自由基加合物在缺血和早期再灌注期间出现，但在基础条件下未出现；自旋加合物的特征是碳中心自由基，这与膜脂质受到氧化攻击一致。自由基形成的直接证据支持了自由基在脑缺血期间组织学损伤发病机制中起作用的假说。
