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Exhaled Nitric Oxide and Pulmonary Oxygen Toxicity Susceptibility

Individual susceptibility to pulmonary oxygen toxicity (PO(2)tox) is highly variable and currently lacks a reliable biomarker for predicting pulmonary hyperoxic stress. As nitric oxide (NO) is involved in many respiratory system processes and functions, we aimed to determine if expired nitric oxide...

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Detalles Bibliográficos
Autores principales: Fothergill, David M., Gertner, Jeffery W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10456729/
https://www.ncbi.nlm.nih.gov/pubmed/37623874
http://dx.doi.org/10.3390/metabo13080930
Descripción
Sumario:Individual susceptibility to pulmonary oxygen toxicity (PO(2)tox) is highly variable and currently lacks a reliable biomarker for predicting pulmonary hyperoxic stress. As nitric oxide (NO) is involved in many respiratory system processes and functions, we aimed to determine if expired nitric oxide (F(E)NO) levels can provide an indication of PO(2)tox susceptibility in humans. Eight U.S. Navy-trained divers volunteered as subjects. The hyperoxic exposures consisted of six- and eight-hour hyperbaric chamber dives conducted on consecutive days in which subjects breathed 100% oxygen at 202.65 kPa. Subjects’ individual variability in pulmonary function and F(E)NO was measured twice daily over five days and compared with their post-dive values to assess susceptibility to PO(2)tox. Only subjects who showed no decrements in pulmonary function following the six-hour exposure conducted the eight-hour dive. F(E)NO decreased by 55% immediately following the six-hour oxygen exposure (n = 8, p < 0.0001) and by 63% following the eight-hour exposure (n = 4, p < 0.0001). Four subjects showed significant decreases in pulmonary function immediately following the six-hour exposure. These subjects had the lowest baseline F(E)NO, had the lowest post-dive F(E)NO, and had clinical symptoms of PO(2)tox. Individuals with low F(E)NO were the first to develop PO(2)tox symptoms and deficits in pulmonary function from the hyperoxic exposures. These data suggest that endogenous levels of NO in the lungs may protect against the development of PO(2)tox.