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Plasma nitrite concentration decreases after hyperoxia‐induced oxidative stress in healthy humans
Author(s) -
Modun Darko,
Krnic Mladen,
Vukovic Jonatan,
Kokic Visnja,
KukocModun Lea,
Tsikas Dimitrios,
Dujic Zeljko
Publication year - 2012
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1111/j.1475-097x.2012.01133.x
Subject(s) - hyperoxia , malondialdehyde , nitrite , oxidative stress , nitric oxide , medicine , vasoconstriction , endocrinology , anesthesia , chemistry , nitrate , organic chemistry , lung
Summary 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, AI x) 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 H g), AI x (from −63 ± 4 to −51 ± 3%) and MDA (from 152 ± 13 to 218 ± 15 n m ) values and a decrease in plasma nitrite (from 918 ± 58 to 773 ± 55 n m ). During the 15‐min recovery phase, plasma nitrite, AI x 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.