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Undersea Hyperb Med. 2013 Jan-Feb;40(1):7-13.

Exhaled nitric oxide and lung function after moderate normobaric hyperoxic exposure.

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  • 1Institute of Medicine, University of Bergen, Bergen, Norway.



Pulmonary oxygen toxicity is associated with inflammatory responses in the airways and alveoli. The purpose of this study was to investigate whether the changes in exhaled nitric oxide (FE(NO)) after exposure to normobaric hyperoxia (NBO), 100% oxygen (O2) at 1 atmosphere absolute (atm abs) for 90 minutes, are associated with changes in lung function.


Eighteen healthy non-smoking subjects were exposed to NBO breathing 100% oxygen and to breathing ambient air, both for 90 minutes on separate days and in random order. Dynamic and static lung volumes, maximal expiratory flow rates, distribution of ventilation including closing volume and slope of phase III of the nitrogen washout curve (delta N2), diffusion capacity (D(L)CO) and FE(NO) were measured before and after the exposures.


The mean reduction in FE(NO) was 20% (SD = 20) after the NBO exposure (p < 0.001). Static and dynamic lung volumes, maximal expiratory flow rates, DLCO and distribution of ventilation were unchanged. No association was found between the changes in the lung function variables and the change in FE(NO).


Unchanged indices of distribution of ventilation and maximal expiratory flow rates indicate no small airways' dysfunction, and unchanged DLCO suggests preserved gas transfer in the lung despite a significant reduction in FE(NO). FE(NO) might be an index of oxygen exposure, but further studies over a wide range of oxygen exposures are necessary to establish the role of FE(NO) as a marker of pulmonary oxygen toxicity.

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