J Asthma Allergy Clin Immunol.
1999 Feb;19(1):19-30.
Ozon-induced airway hyperresponsiveness of rat tracheal smooth muscle
Abstract
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BACKGROUND: Ozone (03) induces airway inflammation and hyperresponsiveness which are
characteristic features of asthma. There have been few studies observing O3-induced
increase in responsiveness of rat airway muscle. Objectives: The aims of this study
were to develop an O3-induced nonallergic asthma model using rat tracheal smooth muscle
(TSM) and to evaluate the role of airway epithelium on the modulation of muscle responsiveness.
METHOD: Five groups of 20 male Sprague-Dawley(SD) rats were exposed to filtered air
including 0.12, 0.5, 1.0, or 2.0 ppm 03 for 1 hour. Thirty minutes after the exposure,
bronchoalveolar lavage (BAL) and isometric contractile responses of the isolated tracheal
ring segments to KCI, acetylcholine (ACh), and electrical field stimulation (EFS) were measured.
RESULTS
The percent age of neutrophils was significantly higher and that of alveolar
macro-phages in BAL fluid was significantly lower in 2.0 ppm O3-exposed rats than in the
control. There were no significant differences in the maximal contractile responses of
TSM to KC1, ACh, EFS and in the sensitivity to ACh (ACh-EC50) and EFS (EFS-EC50) between
the control group and the ozone exposed group. ACh-EC50 and EFS-EC50 were correlated
positively with the percent age of neutrophils and inversely with that of macrophages.
Removal of epithelium significantly increased the sensitivity to ACh in O3-exposed group,
but not in the control group.
CONCLUSION
These findings indicate that O3 induces neutrophilic airway inflammation,
but not an increased sensitivity of TSM to ACh or EFS in SD rats. However, O3-induced
epithelial damage may be associated with increased muscle response.