Central nervous system oxygen toxicity in the resting rat: postponement by intermittent oxygen exposure.

Intermittent O2 breathing is a proven means of delaying pulmonary O2 toxicity during exposure to hyperbaric oxygen. The effect of an intermittent exposure in the pressure range toxic to the CNS was studied. Conscious, unrestrained rats, implanted with cortical EEG electrodes were subjected at 5 and 6 ATA to alternating periods of 7 min O2 and 7 or 10 min of either air, normoxic nitrox, or N2O-air (the latter mixture being equinarcotic to pure O2). Altogether, nearly half of the animals survived 90 min of intermittent breathing, with no grossly abnormal EEG patterns. At that time, labored breathing (associated with mild lung pathology) supervened. In the remaining animals, seizure patterns in the EEG appeared after a mean cumulative O2 breathing time of 20 min (compared to 9 min during a continuous exposure). Forty percent were affected while breathing the alternating mixture (low-PO2 seizures), mostly soon after switching of the gas. The nature of the alternating mixture did not affect the outcome of the high-PO2 seizures nor did the length of the interim periods. Normoxic nitrox increased and N2O-air reduced the incidence of low-PO2 seizures. At 5 ATA only 10% of the animals experienced high-PO2 seizures. While swift reversibility of the toxic process is indicated, the low-PO2 seizures with as yet an undetermined mechanism pose a serious obstacle for intermittent exposures at this pressure range.