Oxygen poisoning in the unanesthetized brain: Correlation of the oxidation-reduction state of pyridine nucleotide with electrical activity

Using light guides and an implanted cannula for excitation of pyridine nucleotide fluorescence and measurement of fluorescence emission and reflectance from the brain surface of unanesthetized rats, the changes in the oxidation-reduction level of pyridine nucleotides induced by hyperbaric oxygen on the brain cortex have been studied in detail. The level of pyridine nucleotide oxidation was little altered by addition of carbon dioxide to the hyperbaric gas mixture, or by perturbation with succinate, but the sequence of events was shortened by the former and lengthened by the latter treatment. Above the level of pyridine nucleotide oxidation induced by hyperbaric conditions, waves of increased oxidation were observed between bursts of seizure activity. Such oxidation cycles are in all respects similar to those seen on application of KCl to the surface of the cortex, and are thought to be due to K⁺ leakage from the cells to the extracellular space. Possible metabolic shifts of the brain in normoxic and hyperbaric conditions are discussed. The changes in the oxidation-reduction level of pyridine nucleotide induced by hyperbaric conditions are interpreted to indicate that under normoxic, conscious conditions the metabolic state of the brain approaches the 'resting' level characterized by the mitochondrial state 4.