We measured plasma nitrite, the biochemical marker of endothelial nitric oxide (^•NO) synthesis, before and after hyperoxia, in order to test the hypothesis that hyperoxia-induced vasoconstriction is a consequence of reduced bioavailability of ^•NO due to elevated oxidative stress.

Ten healthy males breathed 100% normobaric O₂ for 30 min between the 15^th and 45^th min of the 1 h study protocol. Plasma nitrite and malondialdehyde (MDA), arterial stiffness (indicated by augmentation index, AIx) and arterial oxygen (P_tcO₂) pressure were measured in the 1^st, 15^th, 45^th and 60^th minute of the study.

Breathing of normobaric 100% oxygen during 30 min caused an increase of P_tcO₂ (from 75 ± 2 to 412 ± 25 mm Hg), AIx (from −63 ± 4 to −51 ± 3%) and MDA (from 152 ± 13 to 218 ± 15 nmol/L) and a decrease in plasma nitrite (from 918 ± 58 to 773 ± 55 nmol/L). During the 15-min recovery phase the plasma nitrite, AIx and MDA values remained altered.

This study suggests that the underlying mechanism of hyperoxia-induced vasoconstriction may result from reduced ^•NO bioavailability due to elevated and sustained oxidative stress.