Journal of Applied Physiology, Vol 63, Issue 3 1174-1179, Copyright © 1987 by American Physiological Society
Role of the parasympathetic nervous system in airway hyperresponsiveness after ozone inhalation
G. L. Jones, C. G. Lane, P. J. Manning and P. M. O'Byrne
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Airway hyperresponsiveness develops in dogs after ozone inhalation. This
study examined the role of the parasympathetic nervous system in
ozone-induced airway hyperresponsiveness in dogs. Dose-response curves to
acetylcholine (n = 8) and histamine (n = 4) were measured before and after
exposure to ozone (3 ppm for 30 min). The provocative concentration of each
agonist was measured on two randomly assigned days separated by at least 1
wk. On one day a control experiment was performed, and on the other day the
dogs were pretreated with the ganglionic blocker hexamethonium bromide in
doses that block ganglionic transmission. The acetylcholine provocative
concentration decreased on the control day from 5.5 mg/ml (%SE 1.8) before
ozone to 0.5 mg/ml (%SE 2.0) after ozone (P less than 0.0001). After
pretreatment with hexamethonium the acetylcholine provocative concentration
decreased from 9.0 mg/ml (%SE 1.8) before ozone to 1.0 mg/ml (%SE 2.0)
after ozone (P = 0.002). The results were similar when histamine was used
as the agonist. Therefore, ganglionic blockade does not prevent airway
hyperresponsiveness after ozone inhalation, and a parasympathetic reflex
mechanism is not responsible for airway hyperresponsiveness after ozone
inhalation in dogs.
