Improvement of postischemic dopaminergic dysfunction by edaravone, a free radical scavenger.

Effects of a free radical scavenger, edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), on ischemia/reperfusion-induced dysfunctions of rat striatal dopaminergic neurons were examined using in vivo brain microdialysis. During transient forebrain ischemia, dopamine levels in dialysates were elevated 140-fold above controls but rapidly recovered after reperfusion. The increase in dopamine levels induced by high K+ stimulation after reperfusion was far smaller than that of the controls. Pretreatment with edaravone but not post-treatment dose-dependently improved the response to high K+ but not the massive dopamine increase during ischemia. These results suggest that free radicals produced during ischemia play more important roles in ischemia/reperfusion-induced dysfunctions of dopaminergic neurons.