OXYGEN SENSITIVITY OF MITOCHONDRIAL REDOX STATUS AND EVOKED-POTENTIALRECOVERY EARLY DURING REPERFUSION IN POSTISCHEMIC RAT-BRAIN

Inspired oxygen (FiO(2)) was manipulated during the early reperfusion period after global cerebral ischemia (four-vessel occlusion of 20 or 30 min duration) in anesthetized rats. The goal was to determine wheth er oxygen availability during the early reperfusion period alters reco very of mitochondrial redox state and evoked electrical activity. The effectiveness of post-ischemic oxygen treatment was monitored at the t issue level with oxygen sensitive microelectrodes, and at the mitochon drial level by reflection spectrophotometry of the redox state of cyto chrome oxidase. Transiently decreasing FiO(2) from 0.3 to 0.15 limited reperfusion-induced hyperoxygenation and post-ischemic mitochondrial hyperoxidation (PIMHo). Evoked potential recovery was improved by this treatment after 20 min ischemia but not after 30 min ischemia. Increa sing FiO(2) from 0.3 to 1.0 exacerbated PIMHo and tissue hyperoxygenat ion. Transient elevation of tissue oxygen tension after 30 min of glob al ischemia inhibited recovery of evoked potentials. These data sugges t that a period of heightened vulnerability to oxidative stress occurs within the first 10 min of reperfusion after global ischemia. This pe riod is characterized by tissue hyperoxygenation and mitochondrial hyp eroxidation. Limiting oxygen availability during this period may impro ve the outcome while conversely elevating oxygenation may be detriment al. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.