Key result
12-hour normobaric hyperoxia decreases FVC but does not alter airway responsiveness compared to air.
Why the study?
It was unclear whether normobaric hyperoxia alters airway function during the early stage of pulmonary oxygen toxicity in normal subjects.
Does normobaric hyperoxia alter airway function and responsiveness to methacholine in healthy subjects?
Does normobaric hyperoxia alter airway function and responsiveness to methacholine in healthy subjects?
Early normobaric oxygen toxicity causes diminished vital capacity and respiratory symptoms but does not alter airway responsiveness to methacholine.
Hyperoxia may reduce vital capacity without altering methacholine responsiveness in healthy males; leaves open effects in patients or with prolonged exposure.
Airway responsiveness to inhaled cholinergic agonist during the early stage of pulmonary O2 toxicity was examined to determine whether normobaric hyperoxia alters airway function. Eight healthy nonsmoking males with moderate base-line methacholine responsiveness breathed normobaric O2 (greater than or equal to 95%) over 12 h and on another occasion breathed air in an identical protocol. Vital capacity, expiratory flow, airway responsiveness to methacholine, and respiratory symptoms were measured at 0, 4, 8, and 12 h while subjects breathed O2 and 12 h afterwards. After 12 h, forced vital capacity was significantly decreased with O2 breathing but not with air breathing. At 4, 8, or 12 h of exposure and 12 h after exposure, there was no difference in methacholine sensitivity or reactivity between O2 and air-exposure trials. The earliest manifestations of pulmonary normobaric O2 toxicity in normal adults include diminished vital capacity and the onset of respiratory symptoms, but early O2 toxicity does not produce altered responsiveness to inhaled methacholine.
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Beckett et al. (1988) studied Healthy (n=8). Normobaric hyperoxia (O2) vs. Air was evaluated on Airway responsiveness to methacholine and forced vital capacity. Normobaric hyperoxia for 12 hours significantly decreased forced vital capacity but did not alter airway responsiveness to methacholine compared to air breathing in healthy males.
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