Effect of prolonged normobaric hyperoxia on regional cerebral metabolic rate for glucose in conscious rats.

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.