Endothelial function and stress response after simulated dives to 18 msw breathing air or oxygen

L.A. Madden, B.C. Chrismas, D. Mellor, R.V. Vince, A.W. Midgley, L.R. McNaughton, S.L. Atkin, G. Laden

Research output: Contribution to journalArticlepeer-review


Decompression sickness is caused by gas bubbles released upon decompression. These bubbles have the potential to occlude blood vessels and damage the vascular endothelium. The aim of this study was to quantify damage to the vascular endothelium resulting from decompression by measuring endothelial microparticles (MP) and endothelial function. Methods: Five healthy male volunteers undertook a simulated (hyperbaric chamber) air dive and 1 wk later a second dive breathing 100% oxygen at 283 kPa (18 msw) for 60 min bottom time, decompressed with 5-min stops at 161 kPa (6 msw) and 131 kPa (3 msw). Endothelial function was tested pre- and postdive by reactive hyperemia peripheral artery tonometry (RH-PAT) and CD105 (Endoglin) positive MP were quantified by flow cytometry. Plasma E- and P-selectin, interleukin-6, and serum cortisol were also quantified. Results: RH-PAT showed a significantly decreased endothelial function post-decompression after breathing air when compared to oxygen (−0.33 ± 0.27 vs. +0.18 ± 0.14). CD105 MP pre- and postdive showed no change on the oxygen dive (460 ± 370 to 360 ± 163), however, they increased after breathing air (440 ± 70 to 1306 ± 359). There was no change in expression of CD105 on MP. Furthermore no changes were observed in plasma E- or P-selectin, IL-6, or serum cortisol. Conclusion: From the data, at least in the time frame involved, there appears to be no detectable physiological/stress response to decompression, rather decompression from breathing air probably caused mechanical damage to the endothelium, resulting in both MP release and a reduction in endothelial function.
Original languageEnglish
Pages (from-to)41-45
JournalAviation, Space and Environmental Medicine
Publication statusPublished - 2010


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