ACUTE INHALATION OF OZONE STIMULATES BRONCHIAL C-FIBERS AND RAPIDLY ADAPTING RECEPTORS IN DOGS

To identify the afferents responsible for initiating the vagally media ted respiratory changes evoked by acute exposure to ozone, we recorded vagal impulses in anesthetized, open-chest, artificially ventilated d ogs and examined the pulmonary afferent response to ozone (2-3 ppm in air) delivered to the lower trachea for 20-60 min. Bronchial C-fibers (BrCs) were the lung afferents most susceptible to ozone, the activity of 10 of 11 BrCs increasing from 0.2 +/- 0.2 to 4.6 +/- 1.3 impulses/ s within 1-7 min of ozone exposure. Ten of 15 rapidly adapting recepto rs (RARs) were stimulated by ozone, their activity increasing from 1.5 +/- 0.4 to 4.7 +/- 0.7 impulses/s. Stimulation of RARs (but not of Br Cs) appeared secondary to the ozone-induced reduction of lung complian ce because it was abolished by hyperinflation of the lungs. Ozone had little effect on pulmonary C-fibers or slowly adapting pulmonary stret ch receptors. Our results suggest that both BrCs and RARs contribute t o the tachypnea and bronchoconstriction evoked by acute exposure to oz one when vagal conduction is intact and that BrCs alone are responsibl e for the vagally mediated tachypnea that survives vagal cooling to 7- degrees-C.