Mechanisms contributing to ozone-induced bronchial hyperreactivity in guinea-pigs.
Pulm Pharmacol
; 5(1): 39-50, 1992.
Article
em En
| MEDLINE
| ID: mdl-1375522
ABSTRACT
The effect of ozone (3 ppm, 15-120 min) on bronchial reactivity in the guinea-pig was studied. Ozone induced marked (6-250-fold) bronchial hyperreactivity (BHR) to a range of inhaled, but not intravenous bronchoconstrictors. The degree of BHR was related to the duration of prior ozone exposure. The glutathione redox status was shifted to a more oxidized state in lung after 120 min ozone treatment, although no changes were found in the energy status of lung tissue, as judged by the concentrations of adenosine phosphates. Ascorbic acid pretreatment prevented BHR induced by 30 min ozone exposure. Neutral endopeptidase inhibitors elicited BHR to both substance P and histamine, but did not further enhance bronchoconstriction to substance P after ozone exposure for 120 min. Neither mepyramine, fentanyl, indomethacin nor a 5-lipoxygenase inhibitor (BW B70C), given prior to ozone exposure prevented the induction of BHR to histamine. Atropine or bilateral vagotomy reduced BHR after a 120-min, but not 30-min exposure to ozone. We conclude that in the guinea-pig, ozone induces non-specific, route-dependent BHR by oxidative injury, reducing airway NEP activity and enhancing the cholinergic and peptidergic component to bronchoconstriction. Neither cyclooxygenase nor 5-lipoxygenase products appear to play a role in ozone-induced BHR in this animal model.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Ozônio
/
Broncoconstrição
/
Hiper-Reatividade Brônquica
Limite:
Animals
Idioma:
En
Revista:
Pulm Pharmacol
Assunto da revista:
FARMACOLOGIA
Ano de publicação:
1992
Tipo de documento:
Article
País de afiliação:
Reino Unido