Brain energy metabolism of the conscious rat exposed to various physiological and pathological situations.
Using a time-sharing fluorometer-reflectometer, pyridine nucleotide (NADH) and flavoprotein (Fp) fluorescence, as well as reflected light at the excitation wavelength, were measured and correlated with the electrical activity of an awake cerebral cortex. Exposure of the rat to a nitrogen atmosphere (anoxia) led to an increase in signals representing the reduction of pyridine nucleotides and flavins, with very similar kinetics. Inducement of partial ischemia by bilateral carotid artery ligation led to an increase in NADH, accompanied by a very small effect on the electrical activity (ECoG). In most animals, 2-3h after ligation, the ECoG  became flat or depressed. Exposure of this ischemic cerebral cortex to KC1 solution caused depression of the electrical activity without metabolic response probably due to the limitation of oxygen supply. The metabolic state of an awake cerebral cortex was identified by exposing the brain to various levels of  oxygen, epileptoform activity, spreading depression, hyperbaric pressure of oxygen and an uncoupler. From our results we conclude that the awake cerebral cortex is close to the resting state, state 4, rather than to the active state, state 3.
D000818:Animals; D001921:Brain / Q000098:blood supply; D002540:Cerebral Cortex / Q000378:metabolism*; D003243:Consciousness; D004734:Energy Metabolism; D005420:Flavoproteins / Q000378:metabolism; D006931:Hyperbaric Oxygenation; D000860:Hypoxia / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism; D008297:Male; D009243:NAD / Q000378:metabolism; D051381:Rats
D005420:Flavoproteins; D009243:NAD