| Summary: | Individual susceptibility to pulmonary oxygen toxicity (PO<sub>2</sub>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<sub>E</sub>NO) levels can provide an indication of PO<sub>2</sub>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<sub>E</sub>NO was measured twice daily over five days and compared with their post-dive values to assess susceptibility to PO<sub>2</sub>tox. Only subjects who showed no decrements in pulmonary function following the six-hour exposure conducted the eight-hour dive. F<sub>E</sub>NO decreased by 55% immediately following the six-hour oxygen exposure (<i>n</i> = 8, <i>p</i> < 0.0001) and by 63% following the eight-hour exposure (<i>n</i> = 4, <i>p</i> < 0.0001). Four subjects showed significant decreases in pulmonary function immediately following the six-hour exposure. These subjects had the lowest baseline F<sub>E</sub>NO, had the lowest post-dive F<sub>E</sub>NO, and had clinical symptoms of PO<sub>2</sub>tox. Individuals with low F<sub>E</sub>NO were the first to develop PO<sub>2</sub>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<sub>2</sub>tox.
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