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Department of Environmental Health Sciences, The Johns Hopkins University, Baltimore, Maryland 21205
Bronchoalveolar lavage (BAL) of canine
peripheral airways was performed at various times after
hyperventilation, and BAL fluid (BALF) cell and mediator data were used
to evaluate two hypotheses: 1)
hyperventilation-induced mucosal injury stimulates mediator production,
and 2) mucosal damage is correlated
with the magnitude of hyperventilation-induced bronchoconstriction. We
found that epithelial cells increased in BALF immediately after a 2- and a 5-min dry air challenge (DAC). Prostaglandins
D2 and
F2
and thromboxane
B2 were unchanged immediately
after a 2-min DAC but were significantly increased after a 5-min DAC.
Leukotriene C4,
D4, and
E4 did not increase until 5 min
after DAC. Hyperventilation with warm moist air did not alter BALF
cells or mediators and caused less airway obstruction that occurred
earlier than DAC. BALF epithelial cells were correlated with mediator
release, and mediator release and epithelial cells were correlated with
hyperventilation-induced bronchoconstriction. These observations are
consistent with the hypothesis that hyperventilation-induced mucosal
damage initiates peripheral airway constriction via the release of
biochemical mediators.
airway resistance; exercise-induced asthma; leukotrienes; prostaglandins; thromboxane
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