Plasma nitrite concentration decreases after hyperoxia-induced oxidative stress in healthy humans.

The aim of this study was to measure 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 caused by elevated oxidative stress. Ten healthy men breathed 100% normobaric O(2) for 30 min between 15th and 45th min of the 1-h study protocol. Plasma nitrite and malondialdehyde (MDA), arterial stiffness (indicated by augmentation index, AIx) and arterial oxygen (P(tc)O(2)) pressure were measured at 1st, 15th, 45th and 60th minute of the study. Breathing of normobaric 100% oxygen during 30 min caused an increase in P(tc)O(2) (from 75 ± 2 to 412 ± 25 mm Hg), AIx (from -63 ± 4 to -51 ± 3%) and MDA (from 152 ± 13 to 218 ± 15 nm) values and a decrease in plasma nitrite (from 918 ± 58 to 773 ± 55 nm). During the 15-min recovery phase, plasma nitrite, AIx and MDA values remained altered. This study suggests that the underlying mechanism of hyperoxia-induced vasoconstriction may involve reduced (•)NO bioavailability caused by elevated and sustained oxidative stress.