Mucosal injury and eicosanoid kinetics during hyperventilation-induced bronchoconstriction

Bronchoalveolar lavage (BAL) of canine peripheral airways was performed at various times after hyperventilation, and BAL fluid (BALF) cell and mediato r data were used to evaluate two hypotheses: 1) hyperventilation-induced mu cosal injury stimulates mediator production, and 2) mucosal damage is corre lated with the magnitude of hyperventilation-induced bronchoconstriction. W e found that epithelial cells increased in BALF immediately after a 2- and a 5-min dry air challenge (DAC). Prostaglandins D-2 and F-2 alpha and throm boxane B-2 were unchanged immediately after a 2-min DAC but were significan tly increased after a 5-min DAC. Leukotriene C-4, D-4, and E-4 did not incr ease until 5 min after DAC. Hyperventilation with warm moist air did not al ter BALF cells or mediators and caused less airway obstruction that occurre d earlier than DAC. BALF epithelial cells were correlated with mediator rel ease, and mediator release and epithelial cells were correlated with hyperv entilation-induced bronchoconstriction. These observations are consistent w ith the hypothesis that hyperventilation-induced mucosal damage initiates p eripheral airway constriction via the release of biochemical mediators.