A comparison of factors involved in the development of central nervous system and pulmonary oxygen toxicity in the rat.

Central nervous system oxygen toxicity (CNS-OT) can occur in humans at pressures above 2atmospheres absolute (ATA), and above 4.5ATA in the rat. Pulmonary oxygen toxicity appears at pressures above 0.5ATA. We hypothesized that exposure to mild HBO following extreme exposure might provide protection against CNS, but not pulmonary oxygen toxicity. We measured the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), and nitrotyrosine and nNOS levels in the brain and lung in the following groups: (1) Sham rats, no pressure exposure (SHAM); (2) Exposure to 6ATA oxygen for 60% of latency to CNS-OT (60%LT); (3) Exposure to 6ATA for 60% of latency to CNS-OT, followed by 20min at 2.5ATA for recovery (REC); (4) Exposure to 6ATA for 60% of latency to CNS-OT, followed by 20min at 2.5ATA oxygen and a subsequent increase in pressure to 6ATA until the appearance of convulsions (CONV); (5) Control rats exposed to 6ATA until the appearance of convulsions (C). SOD and CAT activity were reduced in both brain and lung in the REC group. GPX activity was reduced in the hippocampus in the REC group, but not in the cortex or the lung. nNOS levels were reduced in the hippocampus in the REC group. Contrary to our hypothesis, no difference was observed between the brain and the lung for the factors investigated. We suggest that at 2.5ATA and above, CNS and pulmonary oxygen toxicity may share similar mechanisms.