Abstract
Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium–oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29–48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.
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This work was supported by Stolt-Halliburton Joint Venture (SHJV), The Petroleum Safety Authority Norway (PSA), Esso Norge, Norsk Hydro ASA and Statoil ASA.
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Thorsen, E., Segadal, K., Stuhr, L.E.B. et al. No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in \( P_{{{{\rm O}}_{{{\rm 2}}} }} \) during decompression. Eur J Appl Physiol 98, 270–275 (2006). https://doi.org/10.1007/s00421-006-0276-8
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DOI: https://doi.org/10.1007/s00421-006-0276-8