PERSISTENT SMALL-AIRWAYS DYSFUNCTION AFTER EXPOSURE TO HYPEROXIA

To assess the contribution of hyperoxia to reduced pulmonary function after a deep saturation dive, a shallow saturation dive to a pressure of 0.25 MPa with the same profile of hyperoxic exposure as in a deep s aturation dive to 3.7 MPa was conducted. The Po-2 was 40 kPa, with per iods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. Seven submariners and one professional diver aged 22-2 7 yr participated. Pulmonary function, including static and dynamic lu ng volumes and flows and transfer factor for carbon monoxide (TL(co)), were measured twice before, immediately after, 1 mo after, and 1 and 3 yr after the dive. As reported previously, there was a significant r eduction in TL(co) and in maximal expiratory flow rates at low lung vo lumes immediately after the dive. At the follow-up examinations 1 and 3 yr after, there was no recovery of the maximal expiratory flow rates . Forced midexpiratory flow rate was still reduced by 8.7 +/- 5.6% (P < 0.05) and 9.3 +/- 7.1% (P < 0.01), respectively. Forced expired volu me in 1 s and forced vital capacity were not significantly reduced. Th ere was a complete recovery of the TL(co) The findings are consistent with the studies indicating development of airway obstruction in diver s, and the findings indicate that exposure to hyperoxia contributes to this effect.