Hyperoxia inhibits stimulated superoxide release by rat alveolar macrophages

Factors responsible for the loss of respiratory burst capacity (stimulated extracellular O2-. release) of alveolar macrophages (AM) exposed to prolonged hyperoxia were assessed. Specific pathogen-free rats were exposed to 1 ATA O2 for 24-72 h, and lungs of survivors lavaged. Release of O2-. by cells...

Full description

Saved in:
Bibliographic Details
Published inJournal of applied physiology: respiratory, environmental and exercise physiology Vol. 53; no. 3; p. 685
Main Authors Forman, H J, Williams, J J, Nelson, J, Daniele, R P, Fisher, A B
Format Journal Article
LanguageEnglish
Published United States 01.09.1982
Subjects
Animals
Cell Membrane - drug effects
Cells, Cultured
In Vitro Techniques
Macrophages - drug effects
Macrophages - metabolism
Male
Neutrophils - drug effects
Oxygen - blood
Oxygen - metabolism
Oxygen - pharmacology
Pulmonary Alveoli - cytology
Pulmonary Alveoli - metabolism
Rats
Rats, Inbred Strains
Superoxides - metabolism
Online AccessGet more information

Cover

More Information
Summary:Factors responsible for the loss of respiratory burst capacity (stimulated extracellular O2-. release) of alveolar macrophages (AM) exposed to prolonged hyperoxia were assessed. Specific pathogen-free rats were exposed to 1 ATA O2 for 24-72 h, and lungs of survivors lavaged. Release of O2-. by cells after addition of concanavalin A, which stimulated AM but not polymorphonuclear leukocytes (PMN), or digitonin, which stimulated both cell types, was measured using cytochrome c reduction +/- superoxide dismutase. O2-. release by AM declined 47.2% (P less than 0.05) after 24 h of hyperoxia and 100% after 60 h. Percent PMN in the lavage was less than 3% at 0-36 h but increased to 16% at 48 h and to 44% at 72 h. Although addition of PMN to AM in vitro caused inhibition of AM O2-. release, the percent PMN required for inhibition was not reached in vivo until after a significant decline in AM O2-.-releasing capacity had already occurred. Cell-free lavage fluid from either control or hyperoxic rats did not affect AM O2-. release. AM in culture for 24 h in hyperoxia lost 76.7% (P less than 0.005) of O2-.-releasing capacity vs. cells incubated in 20% O2, although dye exclusion was unaffected. The results indicate that the major cause of loss of AM O2-. release by hyperoxia is a direct effect of O2 on the cells.
ISSN:0161-7567
DOI:10.1152/jappl.1982.53.3.685