A [beta]2-adrenergic agonist inhibits dry air-induced injury in canine
peripheral airways..
Omori, Chiharu, Brian H. Schofield, Wayne Mitzner, and Arthur N.
Freed.
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 2:0057A, 1995.
We examined the effects of a [beta]2-agonist on dry air-induced injury in
canine peripheral airways. Dry air-induced bronchoconstriction (AIB)
was assessed by measuring peripheral airway resistance in
anesthetized dogs. Salbutamol reduced AIB by 75% when compared to
control. Colloidal carbon was used to detect bronchovascular leakage
in contralateral sublobar segments that were pretreated with either
saline or salbutamol. About 87% of the perimeter of bronchi was
damaged after dry air challenge (DAC) in saline treated segments.
Salbutamol reduced mucosal damage by 30% (p<0.05). The mucosa of
bronchioles was not injured. The average goblet/ciliated cell ratio
(G/C: which reflects mucosal perturbation) in bronchi decreased from
0.38 in control to 0.15 in challenged bronchi, and this effect was
also evident in bronchioles. Salbutamol did not affect this
decrement. DAC also caused degranulation of mast cells located below
damaged mucosa, dilation of bronchial vessels, and leakage from
capillaries and venules located below normal ciliated and damaged
mucosa of bronchi. Thus, we conclude that salbutamol attenuates
epithelial damage and AIB, but fails to inhibit either mast cell
degranulation or vascular hyperpermeability.
Received 14 November 1994; accepted in final form 10 February
1995.
APS Manuscript Number A1163-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 February 1995.