Bryna Cr Chrismas

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

INTRODUCTION 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.

The Effect of the Hyperbaric Environment on Heat Shock Protein 72 Expression in Vivo

Heat shock protein 72 (HSP72) is expressed in response to stress and has been demonstrated to follow a diurnal expression pattern within monocytes and is sensitive to changes in core temperature. Numerous studies have shown changes in HSP72 expression within cell lines exposed to hyperbaric conditions. No studies have investigated changes in HSP72 expression in vivo. Six males participated in the study and were exposed to hyperbaric air and hyperbaric oxygen a week apart. Monocyte HSP72 was analyzed by flow cytometry at 09:00, 13:00, 17:00, 21:00 with hyperbaric oxygen or hyperbaric air breathing commencing at 15:00 for 78 min at a pressure of 2.8 ATA. HSP72 under normoxia followed the established trend; however, following the hyperbaric air or oxygen exposure a reduction in detectable HSP72 was observed at 17:00 and 21:00. No changes in core temperature were observed between 13:00 and 21:00 for any condition. The data show that HSP72 expression is impaired following hyperbaric air (HA) exposure, when compared with control or hyperbaric oxygen (HO) exposure.