Cutaneous exposure to hypoxia does not affect skin perfusion in humans.

Aim: Experiments have indicated that skin perfusion in mice is sensitive to reductions in environmental O ₂ availability. Specifically, a reduction in skin-surface PO ₂ attenuates transcutaneous O ₂ diffusion, and hence epidermal O ₂ supply. In response, epidermal HIF-1α expression increases and facilitates initial cutaneous vasoconstriction and subsequent nitric oxide-dependent vasodilation. Here, we investigated whether the same mechanism exists in humans.
Methods: In a first experiment, eight males rested twice for 8 h in a hypobaric chamber. Once, barometric pressure was reduced by 50%, while systemic oxygenation was preserved by O ₂ -enriched (42%) breathing gas (Hypoxia _Skin ), and once barometric pressure and inspired O ₂ fraction were normal (Control ₁ ). In a second experiment, nine males rested for 8 h with both forearms wrapped in plastic bags. O ₂ was expelled from one bag by nitrogen flushing (Anoxia _Skin ), whereas the other bag was flushed with air (Control ₂ ). In both experiments, skin blood flux was assessed by laser Doppler on the dorsal forearm, and HIF-1α expression was determined by immunohistochemical staining in forearm skin biopsies.
Results: Skin blood flux during Hypoxia _Skin and Anoxia _Skin remained similar to the corresponding Control trial (P = 0.67 and P = 0.81). Immunohistochemically stained epidermal HIF-1α was detected on 8.2 ± 6.1 and 5.3 ± 5.7% of the analysed area during Hypoxia _Skin and Control ₁ (P = 0.30) and on 2.3 ± 1.8 and 2.4 ± 1.8% during Anoxia _Skin and Control ₂ (P = 0.90) respectively.
Conclusion: Reductions in skin-surface PO ₂ do not affect skin perfusion in humans. The unchanged epidermal HIF-1α expression suggests that epidermal O ₂ homoeostasis was not disturbed by Hypoxia _Skin /Anoxia _Skin , potentially due to compensatory increases in arterial O ₂ extraction.
(© 2016 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)