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, E. E. Daniel

Research output: Contribution to journalArticlepeer-review


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 determined 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 of 0.66 mg/ml after O3 (P < 0.0001). The acetylcholine provocative concentration increased slightly after control inhalation to dry room air. Airway smooth muscle showed increased responses to both eletrical 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.

Original languageEnglish
Pages (from-to)57-64
Number of pages8
JournalJournal of Applied Physiology
Issue number1
Publication statusPublished - 1 Jan 1988
Externally publishedYes


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