The term “normobaric oxygen paradox” (NOP), describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as oxygen shortage, and resulting in up-regulation of the Hypoxia-inducible factor 1α (HIF-1α) transcription factor activity. The molecular characteristics of this response have not been yet fully characterized. Herein, we report the activation time trend of oxygen-sensitive transcription factors in human peripheral blood mononuclear cells (PBMCs) obtained from healthy subjects after one hour of exposure to mild (MH), high (HH) and very high (VHH) hyperoxia, corresponding to 30%, 100%, 140% O2, respectively. Our observations confirm that MH is perceived as a hypoxic stress, characterized by the activation of HIF-1α and Nuclear factor (erythroid-derived 2)-like 2 (NRF2), but not Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB). Conversely, HH is associated to a progressive loss of NOP response and to an increase in oxidative stress leading to NRF2 and NF-kB activation, accompanied by the synthesis of glutathione (GSH). After VHH, HIF-1α activation is totally absent and oxidative stress response, accompanied by NF-κB activation, is prevalent. Intracellular GSH and Matrix metallopeptidase 9 (MMP-9) plasma levels parallel the transcription factors activation pattern and remain elevated throughout the observation time. In conclusion, our study confirms that, in vivo, the return to normoxia after MH is sensed as a hypoxic trigger characterized by HIF-1α activation. On the contrary, HH and VHH induce a shift toward an oxidative stress response, characterized by NRF2 and NF-κB activation in the first 24 h post exposure.

Clinical symptoms of spinal cord DCS and their initial course before admission to the hyperbaric center should be considered as major prognostic factors in recovery. A new severity score is proposed to optimize the initial clinical evaluation for spinal cord DCS.

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G ERMONPRE P, PONTIER J-M, GEMPP E, BLATTEAU J-E, DENEWETH S, LAFÉRE P, MARRONIIntroduction: The preconditioning of divers to reduce post-dive decompression sickness (DCS) has gained increased interest in diving medical research over the last few years. The benefi cial effects of physical exercise, oxygen breathing, hyperbaric exposure, heat exposure, hyperhydration, or nitroglycerin administration before the dive are only a few examples of ongoing research. In this work, we investigated the effects of pre-dive whole-body vibration on post-dive bubble formation. Methods: Following French Navy standard dive procedures, 14 healthy male military divers performed 2 identical dives 1 wk apart to 30 m of seawater (msw) for 30 min. One of the dives was randomly preceded by a 30-min whole-body vibration session (frequencies 35-40 Hz) 1 h before the dive. Post-dive bubbles were measured precordially 30, 60, and 90 min after the dive and were graded according to the Kissman Integrated Severity Score (KISS) protocol, with and without knee fl exing. Arterial endothelial function was measured before and after vibration using fl ow mediated dilation (FMD) measurement. Results: A signifi cant reduction in bubble scores was observed after the " vibration " dive. Conclusion: As there was no observed change in FMD after vibration, we do not believe a nitric oxide mediated mechanism is involved; rather, a mechanical dislodgement or enhanced lymphatic elimination of gas nuclei is hypothesized.