Fluorometry and dual-wave-length spectrophotometry were used to detect transitory shifts in the redox state of mitochondrial NADH and cytochrome aa3 in the exposed cerebral cortex of anesthetized paralyzed cats as seizures were induced with pentylenetetrazol. In normotensive animals, NADH and cytochrome aa3 oxidation accompany the seizures, but when the mean arterial pressure (MAP) is reduced to 40.2 +/- 1.1% of the base line by hemorrhaging, the NADH fluorescence response converts to a biphasic oxidation-reduction sequence. In extreme hypotension (MAP lowered to an average of 28%), only NAD reduction transients are observed with seizures, and cytochrome aa3 is oxidized irrespective of the low MAP. Our data show that a reversible perfusion impairment, perhaps inhomogeneous in its distribution, appears in the cortex at the 40% MAP level and modifies electron flux in the respiratory chain between NADH and cytochrome aa3, and uniform oxygen insufficiency is an unlikely cause for the reversal of NADH oxidation toward reduction during seizures under hypovolemic conditions.