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This article is part of the supplement: 18th Scientific Symposium of the Austrian Pharmacological Society (APHAR)

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

Darko Modun1*, Mladen Krnić2, Jonatan Vuković1, Višnja Kokić1, Lea Kukoč-Modun3, Dimitrios Tsikas4 and Zeljko Dujić5

Author Affiliations

1 Department of Pharmacology, School of Medicine, University of Split, 21000 Split, Croatia

2 Department of Endocrinology, University Hospital Split, 21000 Split, Croatia

3 Department of Analytical Chemistry, Faculty of Chemistry and Technology, University of Split, 21000 Split, Croatia

4 Institute of Clinical Pharmacology, Hannover Medical School, 30625 Hannover, Germany

5 Department of Physiology, School of Medicine, University of Split, 21000 Split, Croatia

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BMC Pharmacology and Toxicology 2012, 13(Suppl 1):A88  doi:10.1186/2050-6511-13-S1-A88

The electronic version of this article is the complete one and can be found online at:

Published:17 September 2012

© 2012 Modun et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 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.


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.


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