Plasma nitrite concentrations decrease after hyperoxia-induced oxidative stress in healthy humans

This is the authors' abstract. We don't add key points for this paper.

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 O 2 for 30 min between the 15 and 45 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 in the 1 , 15 , 45 and 60 minute of the study. Breathing of normobaric 100% oxygen during 30 min caused an increase of 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 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.