Journal of Applied Physiology, Vol 64, Issue 2 605-610, Copyright © 1988 by American Physiological Society
Prolonged increased responsiveness of canine peripheral airways after exposure to O3
W. S. Beckett, A. N. Freed, C. Turner and H. A. Menkes
Division of Environmental Physiology, School of Public Health, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Because it is relatively insoluble, the oxidant gas O3 may penetrate to
small peripheral airways when it is inhaled. Increased responsiveness in
large airways after O3 breathing has been associated with the presence of
inflammatory cells. To determine whether O3 produces prolonged
hyperresponsiveness of small airways associated with the presence of
inflammatory cells, we exposed the peripheral lungs of anesthetized dogs to
1.0 ppm O3 for 2 h using a wedged bronchoscope technique. A contralateral
sublobar segment was simultaneously exposed to air as a control. In the
O3-exposed segments, collateral resistance (Rcs) was increased within 15
min and remained elevated approximately 150% throughout the 2-h exposure
period. Fifteen hours later, the base-line Rcs of the O3-exposed sublobar
segments was significantly elevated, and these segments demonstrated
increased responsiveness to aerosolized acetylcholine (100 and 500
micrograms/ml). There were no differences in neutrophils, mononuclear
cells, or mast cells (numbers or degree of mast cell degranulation) between
O3 and air-exposed airways at 15 h. The small airways of the lung periphery
thus are capable of remaining hyperresponsive hours after cessation of
localized exposure to O3, but this does not appear to be dependent on the
presence of inflammatory cells in the small airway wall.
