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To assess the residual effects of transient cerebral ischemia on mitochondrial oxidative metabolic function, changes in the reduction/oxidation state of cytochrome a,a3 and relative local blood volume were measured in situ from the exposed cerebral surface of rat brain before and after 10 minutes of carotid artery ligation. During the ischemic interval, cytochrome a,a3 became reduced and electrocortical activity was abolished. During the first 20 minutes of reperfusion cytochrome a,a3 was hyperoxidized beyond baseline with eventual recovery to the original steady state. Electrocortical activity returned more slowly. Increased energy demand induced by electrical stimulation of the cortex produced transient oxidation of cytochrome a,a3. The amplitude of this oxidative response was decreased during the first 30 minutes of reperfusion. During the first 2 hours of reperfusion the time required for re-reduction of the oxidative response was lengthened despite the recovery of baseline mitochondrial redox state. These data demonstrate residual metabolic dysfunction after transient ischemia not apparent under "resting" conditions but evident when the system is required to perform additional "work." We speculate this metabolic dysfunction could be due to relative substrate limitation.

Disparate recovery of resting and stimulated oxidative metabolism following transient ischemia.