Acid aspiration increases sensitivity to increased ambient oxygen concentrations

Departments of 1  Anesthesiology, 2  Microbiology, and 3  Pharmacology, State University of New York at Buffalo, Buffalo 14214; and 4  Department of Pediatrics, University of Rochester, Rochester, New York 14642 Previously we have demonstrated that prolonged exposure to 100% ambient oxygen leads to...

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Bibliographic Details
Published in:American journal of physiology. Lung cellular and molecular physiology 2000-06, Vol.278 (6), p.1240-L1247
Main Authors: Knight, Paul R, Kurek, Carlos, Davidson, Bruce A, Nader, Nader D, Patel, Alka, Sokolowski, June, Notter, R. H, Holm, Bruce A
Format: Article
Language:English
Subjects:
Air
Animals
Drug Resistance
Hydrochloric Acid - administration & dosage
Hydrochloric Acid - pharmacology
Lung - drug effects
Lung - metabolism
Osmolar Concentration
Oxygen - poisoning
Pneumonia, Aspiration - mortality
Pneumonia, Aspiration - physiopathology
Pulmonary Surfactants - metabolism
Rabbits
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Summary:Departments of 1  Anesthesiology, 2  Microbiology, and 3  Pharmacology, State University of New York at Buffalo, Buffalo 14214; and 4  Department of Pediatrics, University of Rochester, Rochester, New York 14642 Previously we have demonstrated that prolonged exposure to 100% ambient oxygen leads to a marked loss in functional lung volume and lung compliance, hypoxemia, 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 following experimental gastric acid aspiration. Mild hypoxemia, but no changes in mortality, lung volume, lung compliance, surfactant metabolism, or edema formation occurred after 24 h of normoxia postacid aspiration. Conversely, a relatively short (24-h) exposure to 50% oxygen after acid aspiration results in increased pulmonary edema, physical signs of respiratory distress, and mortality, as well as decreased arterial oxygenation, lung volume, lung compliance, and type II alveolar cell surfactant synthesis. These results suggest that acid aspiration alters the "set point" for oxygen toxicity, possibly by "priming" cells through activation of inflammatory pathways. This pathogenic mechanism may contribute to the progression of aspiration pneumonia to ARDS. aspiration pneumonia; acute respiratory distress syndrome; oxidant stress
ISSN:1040-0605
1522-1504
DOI:10.1152/ajplung.2000.278.6.l1240