Abstract

Previous studies have shown airway hyperreactivity in guinea pigs induced by ozone concentrations from 1 to 4 ppm for periods of up to 4 h. Ambient ozone levels only rarely exceed 0.2 ppm in megacities such as Mexico City and normally lie below 0.1 ppm. Here we investigate the effects of an ozone concentration of between 0.3 and 0.45 ppm upon airway function and inflammatory cell influx in guinea pigs. Airway function was monitored in conscious guinea pigs over a 24-h time course following a 2-h ozone exposure. A significant bronchoconstriction was seen as a decrease in specific airway conductance (sG) at 0.25, 0.5, and 4 h postozone, with a recovery to basal aw values after 7 h, which lasted for the following 17 h. Airway reactivity to methacholine and 5-hydroxytryptamine (5-HT), both iv and inhaled, was assessed in anesthetized guinea pigs between 2 and 3 h after an ozone exposure of the conscious animal. A clear ozone-induced airway hyperreactivity was observed as a leftward shift of the doseresponse curve for both methacholine and 5-HT compared with air-exposed controls. Guinea pigs that were sensitized with ovalbumin, however, did not reveal ozoneinduced airway hyperreactivity to methacholine and the hyperreactivity to 5-HT was reduced. This was attributed to an interaction between ozone and the sensitization process, as sensitization per se did not affect airway reactivity. The airway hyperreactivity appeared to be mediated by the vagus nerves, as vagotomized, unsensitized, anesthetized guinea pigs failed to exhibit ozone-induced airway hyperreactivity to either spasmogen. Airways inflammation was apparent from bronchoalveolar lavage of ozoneexposed animals, which revealed a significant influx of inflammatory cells, in particular eosinophils, compared to air-exposed controls. Wet-dry lung weight measurements, however, did not reveal significant edema and/or secretions in the airways of sensitized or unsensitized animals after ozone exposure.

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