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ROLE OF TACHYKININS IN OZONE-INDUCED ACUTE LUNG INJURY
Citation:
Tepper, J., D. Costa, S. Fitzgerald, D.L. Doerfler, AND P.A. Bromberg. ROLE OF TACHYKININS IN OZONE-INDUCED ACUTE LUNG INJURY. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-95/083, 1993.
Description:
To examine the hypothesis that the acute, reversible changes caused by O3 exposure are mediated by techykinin release, guinea pigs were depleted of tachykinins using repeated capsaicin (CAP) injections prior to O3 exposure, in an attempt to prevent O3-induced functional changes. Unexpectedly, CAP pretreatment caused divergent results in the functional responses to O3. Ventilatory, measurements obtained from CAP-pretreated O3-exposed animals (CAP-O3) were exacerbated rather than diminished in comparison to the effect of O3 alone. Similarly, lavage fluid protein (LFP) accumulation was enhanced in the CAP-O3 group compared to the effect of O3-exposed group. In better agreement with our initial hypothesis, the CAP-O3 group was less responsive to histamine aerosol challenge than O3-exposed animals. Additionally, Evans blue dye accumulation, a hallmark of tachykinin release, was increased in O3-exposed animals and the response was partially blocked in the CAP-O3 treatment group. These data suggest that tachykinin-containing sensory fibers are unlikely to mediate the acute effects of O3 exposure on tidal breathing and LFP accumulation, but may play a role in causing post-O3 airway hyperreactivity and protein extravasation into the trachea.