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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.

The regional cerebral metabolic rate for glucose (rCMRgl) was autoradiographically measured in conscious rats during 180–210 min of exposure to 3 atmospheres absolute oxygen (ATA O2), 3 ATA N2-O2 normoxia and air at 1 ATA. The exposure time and oxygen pressure in the present study were purposely matched to a parallel project in human subjects. The electrocorticogram (ECoG) was continuously recorded throughout the exposure. According to the ECoG responses, the oxygen-exposed rats fell into two categories: (1) ‘resistant’ ones, those without changes in ECoG throughout the exposure; and (2) ‘sensitive’ rats, those with changes in EcoG before or during the rCMRgl measurements. The observed ECoG changes were increased slow wave activity in the δ range, which was in some cases followed by paroxysmal electrical discharges. No changes in rCMRgl were observed in oxygen-exposed ‘resistant’ rats as compared to air breathing or N2-O2 normoxic rats at 3 ATA. However, in the ‘sensitive’ rats there were increases in rCMRgl in 8 of the 28 neuroanatomical structures examined as compared to the air breathing and 3 ATA normoxic controls. It is concluded that the increase in rCMRgl are related to the onset of the oxygen-induced preconvulsive changes in ECoG.

The CNS tolerance to prolonged normobaric hyperoxia (NH) was investigated using alterations in regional cerebral metabolic rate for glucose (rCMRgl) as a sensitive measure of brain oxygen poisoning. Conscious rats were continuously exposed either to air or to oxygen for 24 h at atmospheric pressure inside a closed and ventilated environmental chamber. The rCMRgl was measured during ongoing air or oxygen exposures by [14C]2-deoxyglucose (2-DG) autoradiographic technique. No significant difference in the rCMRgl of 29 neuroanatomical structures investigated was found between two groups of air- and oxygen-exposed rats. At the same time however, a significant reduction in the respiratory frequency (f) was observed only in the oxygen-exposed rats. It is suggested that brain energy metabolism is not affected at least up to 24 h NH in conscious rats. The NH-induced reduction in f on the other hand, may be due to alterations in afferent inputs from peripheral and central chemoreceptors or lung stretch receptors. Furthermore, since slight changes in rCMRgl of small neuroanatomical structures are not detectable by limited resolution power of [14C]2-DG autoradiographic technique, a subtle NH-induced damage to central respiratory control mechanisms cannot yet be ruled out.

Hyperbaric oxygenation (HBO) at different pressures and durations of exposure produces an increase in regional cerebral metabolic rate for glucose (rCMRgl) in conscious rats. Pentobarbital anesthesia is known to significantly reduce rCMRgl in rats during air breathing. To test if pentobarbital anesthesia is also effective in reducing HBO-induced increases in rCMRgl, the combined effect of pentobarbital anesthesia and HBO on rCMRgl was autoradiographically measured in 28 neuroanatomical structures. Two groups of rats (11 each) were chronically cannulated in one femoral artery and vein 3 days prior to the experiments. Thirty minutes before the rCMRgl measurements the rats were anesthetized with intravenous injection of 50 mg/kg pentobarbital and exposed to either 1-h air breathing at atmospheric pressure or oxygen at 2 atm absolute. No differences in rCMRgl between oxygen-exposed and air-exposed anesthetized rats were observed in 27 of the 28 neuroanatomical structures examined. The superior olivary nucleus was the only one of the 28 structures showing a significant reduction in rCMRgl following anesthesia and HBO. The possible factors involved in the elimination by anesthesia of the previously observed increases in rCMRgl in conscious rats exposed to HBO are discussed.

Hyperbaric oxygen-induced convulsions in awake unrestrained rats are preceded by electrocorticographic changes including paroxysmal electrical discharges (PED). During oxygen induced convulsions, alterations in regional cerebral metabolic rate for glucose (rCMRgl) were autoradiographically measured and compared with rCMRgl results obtained during pre-convulsive periods in an earlier study. Statistically elevated rCMRgl during oxygen-induced convulsions were found in globus pallidus, substantia nigra, limbic structures, and cerebellar cortex. Significant reductions were found largely in auditory structures and cerebral cortex. This pattern of changes in rCMRgl resembles the pattern of changes during successive PED in the absence of overt convulsions. This similarity may indicate that a common sequence of biochemical changes leads to both oxygen-induced pre-convulsive as well as convulsive electrical discharges.

The regional cerebral metabolic rate for glucose (rCMRgl) in 8-14 week-old, male, albino, Wistar rats, weighing 200-385 g was autoradiographically measured using the [14C]2-deoxyglucose (2-DG) technique. Three age-weight groups of rats were tested: (I) 8-9 weeks old (200-250 g, average 227 +/- 14); (II) 10-11 weeks old (255-300 g, average 280 +/- 15 g); (III) 12-14 weeks old (305-385 g; average 331 +/- 25 g). A gradual reduction in rCMRgl was observed in the older and heavier groups. The reductions were statistically significant in 18/28 investigated structures in group III as compared to group I. Since such significant variation in the investigated age-weight range may affect rCMRgl values obtained in different experiments, it is suggested to use narrow and uniform age-weight groups for experimentation concerning brain metabolic functions.