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.