Effect of furosemide on dry air-induced bronchoconstriction, airway
injury, and microvascular hyperpermeability.
Freed, Arthur N., Varsha Taskar, Brian Schofield, and Chiharu Omori.
Department of Environmental Health Sciences, The Johns Hopkins
University, 615 North Wolfe Street, Baltimore, Maryland 21205, The
First Department of Internal Medicine, Nihon University School of
Medicine, 30-1 Oyaguchikamimachi Itabashiku, Tokyo, 173 Japan
APStracts 3:0379A, 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 2000 ml/min. After
pretreatment with aerosolized saline containing 0.75% DMSO, DAC
increased Rp 72+11% (X+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 prior to DAC, and after one hour 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 towards
enhanced bronchovascular permeability in dry air challenged 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.
Received 29 April 1996; accepted in final form 26 July 1996.
APS Manuscript Number A410-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996