Previously we have demonstrated that prolonged exposure to 100% ambient oxy
gen leads to a marked loss in functional lung volume and lung compliance, h
ypoxemia, and surfactant system abnormalities similar to acute respiratory
distress syndrome (ARDS). However, 50% oxygen administration is believed to
be safe in most clinical settings. In the present study, we have evaluated
the effects of a 24-h exposure to 50% oxygen in rabbits immediately follow
ing experimental gastric acid aspiration. Mild hypoxemia, but no changes in
mortality, lung volume, lung compliance, surfactant metabolism, or edema f
ormation occurred after 24 h of normoxia postacid aspiration. Conversely, a
relatively short (24-h) exposure to 50% oxygen after acid aspiration resul
ts in increased pulmonary edema, physical signs of respiratory distress, an
d mortality, as well as decreased arterial oxygenation, lung volume, lung c
ompliance, and type II alveolar cell surfactant synthesis. These results su
ggest that acid aspiration alters the "set point" for oxygen toxicity, poss
ibly by "priming" cells through activation of inflammatory pathways. This p
athogenic mechanism may contribute to the progression of aspiration pneumon
ia to ARDS.