EFFECT OF DIFFERENT OZONE CONCENTRATIONS ON THE NEUROGENIC CONTRACTION AND RELAXATION OF GUINEA-PIG AIRWAYS

Prejunctional and postjunctional effects of several ozone (O-3) concen trations, including those found in highly polluted cities, were evalua ted in guinea pig airways. Animals bred in O-3-free conditions were ex posed to air or O-3 (0.3, 0.6 or 1.2 ppm) during 4 h, and studied 16-1 8 h later. Tracheal and bronchial rings were studied in organ baths. E lectrical field stimulation (EFS) (100 V, 2 ms, 10 s) was given at inc reasing frequencies (0.25-16 Hz). Some tissues received atropine (2 mu M) and/or propranolol (10 mu M). Concentration-response curves to car bachol, isoproterenol, nitroprusside, and substance P were constructed . In tracheas, almost all O-3 concentrations decreased the relaxation at low EFS frequencies, but had no effect on the propranolol-resistant (i-NANC) relaxation, suggesting that only adrenergic relaxation was a ffected. This was a prejunctional effect, since O-3 did not modify the responses to isoproterenol. Relaxation induced by a nitric oxide (NO) donor, nitroprusside, was not affected by O-3, which agrees with the lack of O-3-effect on i-NANC system. O-3 did not modify the EFS-induce d e-NANC contraction in atropine-treated bronchi, nor the contraction caused by exogenous substance P. By contrast, in bronchi without atrop ine, 1.2 ppm O-3 increased the e-NANC contraction induced by the highe st EFS (16 Hz). O-3 increased the maximum responses to carbachol in tr acheas (1.2 ppm) and bronchi (0.6 and 1.2 ppm). In conclusion, we foun d that: a) O-3 decreased adrenergic relaxation in guinea pig tracheas at low EFS frequencies through a prejunctional alteration; b) O-3 did not modify the i-NANC relaxation in tracheas, at least the NO-mediated ; c) O-3 added a cholinergic component to the bronchial slow-phase (e- NANC) contraction evoked by EFS; and d) O-3 enhanced the cholinergic r esponses in trachea and bronchi by a postjunctional mechanism.