Study objectives: To determine if the concentration of nitric oxide (NO) in the lungs increases with hyperpnea by contrasting calculated production (ie, the product of the fractional expired NO concentration [FeNO] and minute ventilation [Ve]) [V̇no] with the amount of NO in equilibrium with the conducting airways (eNOair) and the amount of NO diffusing from the alveoli (eNOalv).
Design: Observational study.
Setting: University teaching hospital.
Participants: Normal subjects.
Interventions: Measurements were made in 16 healthy people during and after 4 min of tidal breathing (10 L/min) and isocapnic hyperventilation of 60 L/min.
Measurements and results: FeNO was measured by collecting the exhaled air during the last minute of each trial and passing it through a chemiluminescence analyzer. The expired NO levels in the plateau phases of slow (30 mL/s) and fast (200 mL/s) single-breath exhalations were also obtained before and after hyperventilation. The Vno (mean ± SEM) increased from 89.8 ± 12.3 to 329.1 ± 36.2 nL/min as V̇e rose (p < 0.001). However, neither the quantities of eNOair nor eNOalv changed with hyperventilation (eNOair range before to after, 34.9 ± 7.7 to 30.9 ± 6.4 parts per billion [ppb], p = 0.96; eNOalv range before to after, 7.3 ± 1.5 to 6.5 ± 1.1 ppb, p = 0.97).
Conclusions: These data demonstrate that the amount of NO in equilibrium with the airway walls and alveoli are not altered by hyperpnea. Rather, the apparent augmentation in V̇no in such circumstances appears to be an arithmetic artifact.