Acute exposure to ozone (O3), one of the major air pollutants in urban areas, induces transient bronchial hyperreactivity, and increased sensitivity of bronchopulmonary C-fiber afferent endings is probably involved (JAP 83:958, 1997). The present study is aimed to determine the effect of O3 exposure on the responses of pulmonary C-fibers to chemical and mechanical stimuli. A total of 31 C-fibers were studied in anesthetized, paralyzed, and open-chest rats. During control, injection of capsaicin (0.5 or 1 μg/kg) abruptly evoked a short burst of discharge (0.77±0.28 imps/s, 2-s average). After acute exposure to O3 (3 ppm for 30 mm), 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 (6.08±0.88 imps/s, P<0.05) immediately after O3 exposure and returned to control in 54±6 min. Similarly, the pulmonary C-fiber response to injection of lactic acid (0.1 mmol/kg) was also elevated after O3 exposure (control: 1.48±0.37 imps/s; after O3: 3.18±0.58 imps/s; n=30; P<0.05). Furthermore, O3 exposure significantly potentiated the C-fibers response to constant-pressure (Pt=30 cmH2O) lung inflation (control: 0.29±0.09 imps/s; after O3: 1.45±0.38 imps/s; n=29; P<0.05). In summary, our results show that the sensitivities of pulmonary C-fiber afferents to chemical and mechanical stimuli are markedly enchanced after acute exposure to O3, suggesting a possible involvement of these afferents in the O3-induced transient bronchial hyperreactivity.
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology