Ozone enhances excitabilities of pulmonary C fibers to chemical and mechanical stimuli in anesthetized rats

Acute exposure to ozone (O₃) enhances pulmonary chemoreflex response to capsaicin, and an increased sensitivity of bronchopulmonary C-fiber afferent endings may be involved. The present study was aimed at determining the effect of O₃ on the responses of pulmonary C fibers to chemical and mechanical stimuli. A total of 31 C fibers were studied in anesthetized, open-chest, and vagotomized rats. During control, right atrial injection of a low dose of capsaicin abruptly evoked a short and mild burst of discharge [0.77 ± 0.28 impulses (imp)/s, 2-s average]. After acute exposure to O₃ (3 parts/million for 30 min), there was no significant change in arterial blood pressure, tracheal pressure, or baseline activity of C fibers. However, the stimulatory effect of the same dose of capsaicin on these fibers was markedly enhanced (6.05 ± 0.88 impulses/s; P < 0.01) and prolonged immediately after O₃ exposure, and returned toward control in 54 ± 6 min. Similarly, the pulmonary C-fiber response to injection of a low dose of lactic acid was also elevated after O₃ exposure. Furthermore, O₃ exposure significantly potentiated the C-fiber response to constant-pressure (tracheal pressure = 30 cmH₂O) lung inflation (control: 0.19 ± 0.07 imp/s; after O₃: 1.12 ± 0.26 imp/s; P < 0.01). In summary, these results show that the excitabilities of pulmonary C-fiber afferents to lung inflation and injections of chemical stimulants are markedly potentiated after acute exposure to O₃, suggesting a possible involvement of these afferents in the O₃-induced changes in breathing pattern and chest discomfort in humans.