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Department of Physiology, University of Kentucky, Lexington, Kentucky 40536
Received 25 February 1997; accepted in final form 8 May 1997.
Wu, Zhong-Xin, Robert F. Morton, and Lu-Yuan Lee. Role
of tachykinins in ozone-induced airway hyperresponsiveness to cigarette
smoke in guinea pigs. J. Appl.
Physiol. 83(3): 958-965, 1997.
Acute exposure to ozone
(O3) induces airway
hyperresponsiveness to various inhaled bronchoactive substances.
Inhalation of cigarette smoke, a common inhaled irritant in humans, is
known to evoke a transient bronchoconstrictive effect. To examine
whether O3 increases airway
responsiveness to cigarette smoke, effects of smoke inhalation
challenge on total pulmonary resistance
(RL) and dynamic lung
compliance (Cdyn) were compared before and after exposure to
O3 (1.5 ppm, 1 h) in anesthetized
guinea pigs. Before O3 exposure,
inhalation of two breaths of cigarette smoke (7 ml) at a low
concentration (33%) induced a mild and reproducible
bronchoconstriction that slowly developed and reached its peak
(
RL = 67 ± 19%, Cdyn = 
29 ± 6%) after a delay of >1 min. After exposure to
O3 the same cigarette smoke
inhalation challenge evoked an intense bronchoconstriction that
occurred more rapidly, reaching its peak
(RL = 620 ± 224%, Cdyn = 35 ± 7%) within 20 s, and was sustained for >2
min. By contrast, sham exposure to room air did not alter the
bronchomotor response to cigarette smoke challenge. Pretreatment with
CP-99994 and SR-48968, the selective antagonists of neurokinin type 1 and 2 receptors, respectively, completely blocked the enhanced
responses of RL and Cdyn to
cigarette smoke challenge induced by
O3. These results show that
O3 exposure induces airway
hyperresponsiveness to inhaled cigarette smoke and that the enhanced
responses result primarily from the bronchoconstrictive effect of
endogenous tachykinins.
neurokinin receptor antagonists; bronchopulmonary C-fibers; inhaled irritants; neurokinin A; substance P; bronchoconstriction
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