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Department of Environmental Health Sciences, The Johns Hopkins University, Baltimore, Maryland 21205; and The First Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173, Japan
Received 29 April 1996; accepted in final form 26 July 1996.
Freed, Arthur N., Varsha Taskar, Brian Schofield, and
Chiharu Omori. Effect of furosemide on hyperpnea-induced airway obstruction, injury, and microvascular leakage. J. Appl. Physiol. 81(6): 2461-2467, 1996.
Furosemide
attenuates hyperpnea-induced airway obstruction (HIAO) in asthmatic
subjects via unknown mechanism(s). We studied the effect of furosemide
on dry air-induced bronchoconstriction, mucosal injury, and
bronchovascular hyperpermeability in a canine model of exercise-induced
asthma. Peripheral airway resistance (Rp) was recorded before and after
a 2-min dry-air challenge (DAC) at 2,000 ml/min. After pretreatment
with aerosolized saline containing 0.75% dimethyl sulfoxide, DAC
increased Rp 72 ± 11% (SE, n = 7) above baseline; aerosolized furosemide
(10
3 M) reduced this
response by ~50 ± 6% (P < 0.01). To assess bronchovascular permeability, colloidal carbon was
injected (1 ml/kg iv) 1 min before DAC, and after 1 h, the vehicle- and
furosemide-treated airways were prepared for morphometric analysis.
Light microscopy confirmed previous studies showing that DAC damaged
the airway epithelium and enhanced bronchovascular permeability.
Furosemide did not inhibit dry air-induced mucosal injury or
bronchovascular hyperpermeability and in fact tended to increase airway
damage and vascular leakage. This positive trend toward enhanced
bronchovascular permeability in DAC canine peripheral airways is
consistent with the hypothesis that furosemide inhibits HIAO in part by
enhancing microvascular leakage and thus counterbalancing the
evaporative water loss that occurs during hyperpnea.
asthma; bronchovascular permeability; goblet cells; hyperpnea-induced bronchoconstriction; mast cells
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