Journal of Applied Physiology
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J Appl Physiol 78: 2169-2179, 1995;
8750-7587/95 $5.00
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Journal of Applied Physiology, Vol 78, Issue 6 2169-2179, Copyright © 1995 by American Physiological Society

ARTICLES

A beta 2-adrenergic agonist inhibits dry air-induced injury in canine peripheral airways

C. Omori, B. H. Schofield, W. Mitzner and A. N. Freed
Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA.

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 approximately 75% compared with control values. Colloidal carbon was used to detect bronchovascular leakage in contralateral sublobar segments that were pretreated with saline or salbutamol. About 87% of the perimeter of bronchi was damaged after dry air challenge in saline-treated segments. Salbutamol reduced mucosal damage by approximately 30% (P < 0.05). The mucosa of bronchioles was not injured. The average goblet-to-ciliated cell ratio (which reflects mucosal perturbation) in bronchi decreased from 0.38 in control bronchi to 0.15 in challenged bronchi, and this effect was also evident in bronchioles. Salbutamol did not affect this decrement. Dry air challenge 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 mast cell degranulation and vascular hyperpermeability.


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