Ozon-induced airway hyperresponsiveness of rat tracheal smooth muscle / 천식및알레르기

ABSTRACT

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.