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Neuropeptides. 2004 Dec;38(6):351-8.

Chlorine inhalation produces nasal airflow limitation in allergic rhinitic subjects without evidence of neuropeptide release.

Author information

1
Upper Airway Biology Laboratory, University of California, San Francisco, Box 0843, San Francisco, CA 94143, USA. dennis3@u.washington.edu

Abstract

BACKGROUND:

Seasonal allergic rhinitic (SAR) subjects are more physiologically reactive to airborne irritants than non-rhinitic (NR) subjects; however the mechanism underlying this difference is unclear.

OBJECTIVE:

We sought to determine whether irritant-induced nasal airflow limitation involves neuropeptide release into nasal lining fluid, and if so, whether such release occurs differentially by rhinitic status.

METHODS:

Eight SAR and 8 NR subjects were exposed to 1.0 ppm chlorine and filtered air in random order during separate visits; exposures were via nasal mask and lasted 15 min. Rhinomanometry was performed before, immediately post-, and 15 min post-exposure. Following a minimum of 2 weeks' time, exposures and symptom reporting were repeated with nasal lavage pre- and post-exposure. Neuropeptides (substance P, cacitonin gene-related protein, vasoactive intestinal peptide, and neuropeptide Y) as well as markers of plasma leakage (albumin and urea) and glandular secretion (lysozyme and 7F10-mucin) were measured using standard methods.

RESULTS:

Cl(2) provocation significantly increased nasal airway resistance in SAR but not NR subjects (p<0.05). Neuropeptide levels in nasal lavage fluid, on the other hand, were unaffected, with the exception of a paradoxical increase in vasoactive intestinal peptide in non-rhinitic controls post-Cl(2) provocation.

CONCLUSIONS:

Irritant-induced nasal airflow limitation is more pronounced among SAR than NR subjects. We could not, however, demonstrate a role for neuropeptide release in the nasal congestive response of SAR subjects.

PMID:
15567471
DOI:
10.1016/j.npep.2004.08.002
[Indexed for MEDLINE]

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