Summary: The isolated urinary bladder of the toad was used to compare the effects on O2 toxicity of 1-min and 5-min intermittent normoxic exposures during a prolonged period of hyperoxic exposure (OHP). Various intermittent exposure schedules were tested at 5 atmospheres (ATA) including 4–1 (4 min 100% O2 followed by l min 4% O2) 6–1, 9–1, 10–5, 15–5, and 20–5. With all schedules tested, intermittent normoxic exposure significantly protected the SCC (active sodium transport) against the inhibition by 5 ATA of O2. Two intermittent schedules (4–1 and 15–5) were tested at 10 ATA using 4% O2 for the reduced O2 pressure exposure. A significant decrease in the rate of SCC inhibition was observed using both intermittent exposure schedules. The observed SCC protection by intermittent exposure (at 5 and 10 ATA) was not entirely a result of the decreased time of exposure to OHP. Four intermittent schedules were tested at 5 ATA, and the effects of intermittent oxygénation on the SCC were compared with the effects of continuous normoxic exposure. During a 5-hr exposure period, no significant SCC stimulation occurred using a 2–1, 4–1, or 9–1 intermittent schedule. Using a 5–5 intermittent schedule, however, a significant stimulation of SCC was observed at 4 and 5 hr. It was concluded that intermittent normoxic exposures as short as l min can afford significant protection against O2 toxicity.Speculation: Pulmonary oxygen toxicity often limits the treatment of respiratory distress syndrome. Intermittent normoxic periods as brief as 1 min can be protective against in vitro oxygen toxicity. This, combined with the previous demonstration that intermittent normoxia is protective against pulmonary oxygen toxicity in man suggests that brief intermittent periods of air breathing might decrease the incidence of bronchopulmonary dysplasia in infants requiring oxygen therapy.
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