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 ‐1 α 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 ‐1 α 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 ‐1 α 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 ‐1 α 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.