The acute and chronic effects of allergic airway inflammation on
pulmonary nitric oxide production.
Mehta, Sanjay, Craig M Lilly, Julie E Rollenhagen, Kathleen J Haley,
Koichiro Asano, and Jeffrey M Drazen.
Pulmonary Division, Brigham and Women_s Hospital, Harvard Medical
School, Boston, MA
APStracts 3:0149L, 1996.
Nitric oxide (NO) is thought to be an important modulator of airway
function in normal and inflamed airways. We investigated the acute
and chronic effects of induced allergic airway inflammation on NO
levels in mixed expired gas and NO synthase (NOS) expression in
guinea pigs and the relationship between airway responses and NO
production. Airway inflammation was induced by repeated aerosolized
antigen exposure and its presence confirmed by bronchoalveolar
lavage. Acute antigen exposure in sensitized animals produced a 5
-fold increase in respiratory resistance over baseline that was
associated with a cotemporal increase in expired NO (17+/-1 to 56+/-8
parts per billion, p<0.01). A continuous subcutaneous infusion
of NG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor
of NOS, markedly decreased expired NO (p<0.01) and resulted in a
significantly greater rise in resistance following antigen challenge
(660+/-60% vs 497+/-42% of baseline in non-L-NAME treated animals,
p<0.05). These data support the hypothesis that endogenous
pulmonary NO production, as reflected by expired NO, has an important
homeostatic role in acute allergic bronchoconstriction.
Received 29 February 1996; accepted in final form 26 August 1996.
APS Manuscript Number L72-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996