Correlation of brain glucose utilization and cortical electrical activity during development of brain oxygen toxicity.

Central nervous system (CNS) oxygen toxicity in rats is characterized by the appearance of alterations in electrical cortical activity (ECoG), followed by the appearance of paroxysmal electrical discharges and finally the onset of clinical convulsions. The correlation between the changes in ECoG and the regional cerebral metabolic rate for glucose (rCMRgl) during progressive oxygen toxicity was studied. Cortical electrodes for ECoG recording and venal arterial cannula for autoradiographic measurement of rCMRgl were chronically implanted. Using [14C]2-deoxyglucose (2-DG), the rCMRgl was measured in conscious unrestrained rats during different periods of exposure to 5 atmospheres absolute oxygen as well as an equivalent normoxic high pressure, while ECoG was continuously recorded and analyzed. A statistically significant increase in rCMRgl in 13 out of 24 investigated brain structures was found during the pre-paroxysmal electrical discharge period. This increase was accompanied by an elevation in slow and a reduction in fast ECoG frequency bands. The largest increase in rCMRgl was found in cerebellar and cerebral cortices, limbic, auditory and visual structures. Following the appearance of the first paroxysmal electrical discharge (FED) some limbic structures and cerebellar cortex showed further increases in rCMRgl, while several auditory and visual structures exhibited a significant decrease. Five atmospheres normoxic pressure had no effect on rCMRgl in any of the brain structures examined. It is concluded that pre-paroxysmal electrical discharge ECoG changes and the onset of the FED during progressive oxygen toxicity are not due to inhibition of brain energy metabolism. The possible mechanisms leading to alterations in rCMRgl during hyperbaric oxygenation are discussed.