Journal of Applied Physiology, Vol 65, Issue 1 57-64, Copyright © 1988 by American Physiological Society
Airway smooth muscle responsiveness from dogs with airway hyperresponsiveness after O3 inhalation
G. L. Jones, P. M. O'Byrne, M. Pashley, R. Serio, J. Jury, C. G. Lane and E. E. Daniel
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Airway hyperresponsiveness occurs after inhalation of O3 in dogs. The
purpose of this study was to examine the responsiveness of trachealis
smooth muscle in vitro to electrical field stimulation, exogenous
acetylcholine, and potassium chloride from dogs with airway
hyperresponsiveness after inhaled O3 in vivo and to compare this with the
responsiveness of trachealis muscle from control dogs. In addition,
excitatory junction potentials were measured with the use of single and
double sucrose gap techniques in both groups of dogs to determine whether
inhaled O3 affects the release of acetylcholine from parasympathetic nerves
in trachealis muscle. Airway hyperresponsiveness developed in all dogs
after inhaled O3 (3 ppm for 30 min). The acetylcholine provocative
concentration decreased from 4.11 mg/ml before O3 inhalation to 0.66 mg/ml
after O3 (P less than 0.0001). The acetylcholine provocative concentration
increased slightly after control inhalation of dry room air. Airway smooth
muscle showed increased responses to both electrical field stimulation and
exogenous acetylcholine but not to potassium chloride in preparations from
dogs with airway hyperresponsiveness in vivo. The increased response to
electrical field stimulation was not associated with a change in excitatory
junctional potentials. These results suggest that a postjunctional
alteration in trachealis muscle function occurs after inhaled O3 in dogs,
which may account for airway hyperresponsiveness after O3 in vivo.
