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

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Background

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.

Methods

Ten healthy males breathed 100% normobaric O2 for 30 min between the 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 (PtcO2) pressure were measured in the 1st, 15th, 45th and 60th minute of the study.

Results

Breathing of normobaric 100% oxygen during 30 min caused an increase of PtcO2 (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.

Conclusions

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

Author information

Correspondence to Darko Modun.

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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Keywords

  • Oxidative Stress
  • Nitric Oxide
  • Biochemical Marker
  • Arterial Stiffness
  • Recovery Phase