2006
DOI: 10.1007/s00421-006-0276-8
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No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in $$ P_{{{{\rm O}}_{{{\rm 2}}} }} $$ during decompression

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 decom… Show more

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Cited by 12 publications
(8 citation statements)
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“…A strong correlation was obtained between the reduction in diffusion capacity of the lung and cumulative hyperoxic exposure [31]. Indeed, no changes in pulmonary function were found after a 240-m saturation dive with a modified dive profile including a reduction in the decompression rate and intermittent reduction of oxygen partial pressure [32]. A slight reduction in forced expiratory flows at lower lung volumes has been obtained after saturation dives, and the decline correlated with cumulative hyperoxic exposure [31].…”
Section: Short-term Effects Of Diving On Lung Functionmentioning
confidence: 86%
“…A strong correlation was obtained between the reduction in diffusion capacity of the lung and cumulative hyperoxic exposure [31]. Indeed, no changes in pulmonary function were found after a 240-m saturation dive with a modified dive profile including a reduction in the decompression rate and intermittent reduction of oxygen partial pressure [32]. A slight reduction in forced expiratory flows at lower lung volumes has been obtained after saturation dives, and the decline correlated with cumulative hyperoxic exposure [31].…”
Section: Short-term Effects Of Diving On Lung Functionmentioning
confidence: 86%
“…Angiotensin II (Ang II) is produced by the conversion of Angiotensin I (ANG I) by the angiotensin converting enzyme (ACE), an enzyme which is abundant in the lungs, bound to endothelial cells and is also found in many other organs including the kidney. Increased levels of serum ACE have been reported after decompression and at even higher levels following DCS (Thorsen et al, 2006 ). Although not the only peptide formed by RAAS, Ang II is the major active metabolite and exerts its effects via AT1 and AT2 receptors.…”
Section: Introductionmentioning
confidence: 99%
“…ANG II is produced by the conversion of ANG I by the angiotensin-converting enzyme (ACE). Increased levels of serum ACE have been reported after decompression and at even higher levels following DCS (34).…”
mentioning
confidence: 99%