Open AccessRespiratory tract inflammation during the induction of chronic bronchitis in rats: role of C‐fibres
Author(s) -
Long N.C.,
Abraham J.,
Kobzik L.,
Weller E.A.,
Krishna Murthy G.G.,
Shore S.A.
Publication year - 1999
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.1999.14a10.x
Subject(s) - capsaicin , chronic bronchitis , respiratory tract , medicine , inflammation , respiratory system , bronchitis , bronchoalveolar lavage , stimulation , ventilation (architecture) , anesthesia , tidal volume , endocrinology , lung , receptor , engineering , mechanical engineering
The hypothesis that chronic stimulation of C‐fibres by inhaled irritants contributes to the inflammatory changes that occur during the development of chronic bronchitis was tested. The effect of neonatal capsaicin pretreatment on the development of respiratory tract inflammation was examined in a rat model of chronic bronchitis induced by SO 2 exposure. Adult capsaicin‐ and vehicle‐treated rats were exposed to SO 2 (250 parts per million (ppm) 5 h·day ‐1 ) for one day, 2 weeks or 4 weeks. Nasal (NL), airway (AL) and bronchoalveolar (BAL) lavages were performed and the number and types of cells in the lavage fluids measured. SO 2 ‐induced changes in ventilation were also measured on day 1 of SO 2 exposure and in the 3rd and 5th week of exposure. In the vehicle‐treated rats, neutrophils became elevated in NL after just one day of SO 2 exposure, in AL after 2 weeks, and in the BAL after 4 weeks. In comparison to vehicle animals, more neutrophils were recovered in the AL of capsaicin‐treated rats after one day of SO 2 (p=0.012), and in the BAL after 2 or 4 weeks (p=0.004 and p=0.01, respectively). On day 1, SO 2 caused a transient increase in tidal volume and a sustained decrease in frequency that was not different in capsaicin‐ and vehicle‐treated rats. With continued exposure, these ventilatory responses to SO 2 were attenuated in both groups of rats. These data support the hypothesis that the presence of C‐fibres limits or delays the inflammation that occurs during the development of chronic bronchitis induced by SO 2 exposure. The protective effect of C‐fibres is not the result of ventilatory responses to stimulation of these afferents.