CONTRIBUTION OF HYPEROXIA TO REDUCED PULMONARY-FUNCTION AFTER DEEP SATURATION DIVES

Pulmonary function was measured before and after a 28-day saturation d ive to a pressure of 0.25 MPa in eight subjects. PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 k Pa for the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. A 28-day saturation dive with six subjects to a pressure of 0.15 MPa and a Po, of 21 kPa was used as control. The mea surements included static and dynamic lung volumes and flows, transfer factor for carbon monoxide (TL(CO)), and a cycle ergometer exercise t est. There was a significant reduction in TL(CO) of 9.8 +/- 6.0% (P < 0.001) after the dive when values were corrected for hemoglobin concen tration changes. Effective alveolar volume was unchanged. There was a reduction in forced midexpiratory flow rate of 9.8 +/- 7.0% (P < 0.01) , but forced vital capacity and forced expired volume in 1 s were unch anged. Peak oxygen uptake was reduced by 10.1 +/- 5.3% (P < 0.001). Th ere were no significant changes in any of the lung function variables after the control dive. Exposure to raised PO2 contributes significant ly to the changes in pulmonary function that have been reported after deep saturation dives to pressures of 3.1-4.6 MPa with a similar profi le of oxygen exposure. TL(CO) is apparently a more sensitive index tha n vital capacity for oxygen toxicity.