Ozone-enhanced airway hyperrespomsiveness involves intrinsic airway neurons in ferret trachea.
Wu-ZX; Satterfield-BE; Fedan-JS; Dey-RD
Am J Respir Crit Care Med 2002 Apr; 165(8)(Suppl):A718
Exposure to ozone (O3), a major air pollutant in urban areas, induces airway hyperresponsiveness mediated partly by the release of tachykinins from nerve terminals of intrinsic airway ganglia (Wu et. al., J. Appl. Physiol. 91:371-378, 2001). The purpose of this study was to investigate the possible involvement of intrinsic airway neurons in O3-induced airway hyperresponsiveness. Segments of ferret trachea were exposed in vitro to 2 ppm 03 or air for 1 hr. Reactivity of isolated tracheal smooth muscle strips to methacholine was significantly increased after 03-exposure, as were contractions to electrical field stimulation (EFS). The 03-enhanced responsiveness was maintained in tracheal segments cultured for 24 h, a procedure shown to deplete most sensory nerves while maintaining viability of intrinsic airway neurons. Furthermore, segments of trachea cultured with 3x10-6 M capsaicin for 24h, which completely depletes tachykinins in sensory nerves, did not abolish the 03-enhanced reactivity to cholinergic agonists and EFS. The findings support the hypotheses that 03-induced airway smooth muscle hyperresponsiveness results partly from the activation intrinsic airway neurons. Further, these neurons may be activated by reflexes ot mediators originating in the airway
Electrical-stimulation; Methacholines; Neuropathy; Cholinergic-receptors; Reflexes; Airway-obstruction; Airway-resistance; In-vitro-study
Abstract; Conference/Symposia Proceedings
Research Tools and Approaches; Exposure Assessment Methods
American Journal of Respiratory and Critical Care Medicine, 2002 International Conference, The American Thoracic Society, Atlanta Georgia, May 17-22, 2002