Journal of Applied Physiology
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J Appl Physiol 87: 1724-1733, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 5, 1724-1733, November 1999

Mucosal injury and eicosanoid kinetics during hyperventilation-induced bronchoconstriction

Arthur N. Freed, Yongqiang Wang, Sharron McCulloch, Teresa Myers, and Ryoichi Suzuki

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 F2alpha 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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