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Effect of ozone treatment on airway reactivity and epithelium-derived relaxing factor in guinea pigs.

Authors
Fedan-JS; Millecchia-LL; Johnston-RA; Rengasamy-A; Hubbs-A; Dey-RD; Yuan-LX; Watson-D; Goldsmith-WT; Reynolds-JS; Orsini-L; Dortch-Carnes-J; Cutler-D; Frazer-DG
Source
J Pharmacol Exp Ther 2000 Jun; 293(3):724-734
NIOSHTIC No.
20020666
Abstract
Ozone (O(3)) is toxic to respiratory epithelium and causes airway inflammation and hyperreactivity. To evaluate the role of the epithelium in the development of hyperreactivity, we examined in guinea pigs the effects of inhaled O(3) (3 ppm for 1 h; 0-24 h after exposure) on 1) reactivity to inhaled methacholine (MCh), 2) reactivity of the isolated, perfused trachea (IPT) to MCh, 3) epithelium-derived relaxing factor (EpDRF)-mediated relaxations of IPT induced by mucosal hyperosmolar solutions, 4) neurogenic contraction and relaxation responses, 5) transepithelial potential difference, and 6) microscopic analysis of nitrotyrosine immunofluorescence, substance P fiber density, and tracheal morphology. At 0 h, O(3) caused hyperreactivity to inhaled MCh and mucosally but not serosally applied MCh in IPT (only in the presence of the epithelium) and a decrease in transepithelial potential difference. Inhibition of EpDRF-induced relaxation responses occurred at 2 h. All of these changes returned to control by 12 to 18 h. O(3) had no effect on neurogenic responses. Nitrotyrosine immunofluorescence appeared in the trachea at 0 h in detached epithelial cell ghosts and in intrapulmonary airways by 6 h. Substance P fiber density was elevated in smooth muscle at 0 and 18 h but not in epithelium or lamina propria of intrapulmonary and extrapulmonary bronchi. Loss of cilia and mucosubstances in the mucosa occurred at 0 h; the epithelium became markedly attenuated over 12 to 24 h. A reversible increase in epithelial permeability and a decrease in EpDRF production may contribute to O(3)-induced hyperreactivity to MCh.
Keywords
Laboratory-animals; Animals; Animal-studies; Airway-obstruction; Toxins; Respiratory-system-disorders; Pulmonary-system-disorders
CODEN
JPETAB
CAS No.
10028-15-6
Publication Date
20000601
Document Type
Journal Article
Email Address
jsf2@cdc.gov
Fiscal Year
2000
NTIS Accession No.
NTIS Price
ISSN
0022-3565
NIOSH Division
HELD
Source Name
The Journal of Pharmacology and Experimental Therapeutics
State
WV
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