Journal of Applied Physiology, Vol 57, Issue 5 1480-1488, Copyright © 1984 by American Physiological Society
Pulmonary oxygen toxicity in awake dogs: metabolic and physiological effects
A. L. Harabin, L. D. Homer and M. E. Bradley
Because the pulmonary endothelium is sensitive to O2-induced damage, we
studied in vivo angiotensin-converting enzyme (ACE) activity in the lungs
of 14 catheterized unanesthetized dogs exposed either to air or continuous
100% O2 at 1 ATA. For 5 days, or until the dog died, we measured
physiological variables and lung ACE activity. The metabolic data were
analyzed with a model that accounted for the effect of changes in cardiac
output. Nine dogs breathing O2 lived 88 +/- 21.8 (SD) h and except for
blood O2 tensions were indistinguishible from controls until development of
a terminal response lasting only a few hours. Hemodynamic instability
preceded a precipitous terminal change in blood gas tensions which resulted
in impairment of arterial oxygenation, hypercapnia, and acidosis. Plasma
renin activity increased. The metabolic capacity of the pulmonary
endothelium of O2-exposed animals decreased with time so that after 96 h it
was 50% of the control. That of five control animals did not change with
time. Thus changes in lung ACE activity preceded alterations in
hemodynamics or gas exchange, and the contributions of each are discussed.
