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 O₂ availability. Specifically, a reduction in skin-surface PO₂ attenuates transcutaneous O₂ diffusion, and hence epidermal O₂ 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 O₂-enriched (42%) breathing gas (Hypoxia_Skin), and once barometric pressure and inspired O₂ fraction were normal (Control₁). In a second experiment, nine males rested for 8 h with both forearms wrapped in plastic bags. O₂ was expelled from one bag by nitrogen flushing (Anoxia_Skin), whereas the other bag was flushed with air (Control₂). 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 Control₁ ( P = 0.30) and on 2.3 ± 1.8 and 2.4 ± 1.8% during Anoxia_Skin and Control₂ ( P = 0.90) respectively. Conclusion Reductions in skin-surface PO₂ do not affect skin perfusion in humans. The unchanged epidermal HIF-1 α expression suggests that epidermal O₂ homoeostasis was not disturbed by Hypoxia_Skin/Anoxia_Skin, potentially due to compensatory increases in arterial O₂ extraction. [ABSTRACT FROM AUTHOR]