Key result
Hemorrhagic hypotension to ~40% baseline MAP during seizures alters NADH fluorescence, signaling reversible perfusion impairment.
Why the study?
The effects of seizures on mitochondrial redox states in the cerebral cortex under conditions of hemorrhagic hypotension were not well characterized.
Reversible perfusion impairment in the cortex during hemorrhagic hypotension modifies electron flux in the respiratory chain between NADH and cytochrome aa3 during seizures.
Answers are grounded in this paper and cite their sources.
Reversible cortical perfusion impairment may alter mitochondrial electron flux during seizures; hypothesis-generating in animal models, clinical relevance remains open.
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.
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Hempel et al. (1980) studied Seizures and hemorrhagic hypotension. Hemorrhagic hypotension vs. Normotensive state was evaluated on Transitory shifts in the redox state of mitochondrial NADH and cytochrome aa3. Hemorrhagic hypotension to 40% of baseline mean arterial pressure during seizures converted NADH fluorescence to a biphasic oxidation-reduction sequence, indicating reversible perfusion impairment.
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