Airway edema potentiates airway reactivity.
Brown, Robert H., Elias A. Zerhouni, Wayne Mitzner.
Department of Anesthesiology and Critical Care Medicine, Department
of Radiology, Department of Environmental Health Sciences/Division of
Physiology
APStracts 2:0250A, 1995.
Thickening of the airway wall has been hypothesized to be one of the
mechanisms contributing to airway hyperresponsiveness in asthma. If
such thickening of the wall is internal to the airway smooth muscle
or otherwise causes a decrease in baseline airway caliber, it should
also cause exaggerated airway responsiveness. In the present study,
we used high-resolution computed tomography to directly measure the
changes in the caliber and wall thickness of conducting airways
following aerosol histamine challenge before and after normal saline
volume loading. On separate days each of five anesthetized dogs
received either a baseline aerosol challenge of 3 mg/ml of
aerosolized histamine for five breaths or the same aerosol challenge
immediately following a 100 ml/kg bolus of normal saline infused over
a 10 minute period. Baseline aerosol histamine challenge decreased
airway area to 71+/-2% (mean+/-sem) of control (p<0.05).
Intravenous administration of 100 ml/kg of normal saline increased
wall area by decreasing airway lumenal area to 78+/-3% of control
(p<0.01), with no change in outer airway area. Aerosol histamine
challenge superimposed on this engorgement with normal saline
challenge further decreased airway lumen area to 54+/-3% of control
(P<0.01). Quantitative modeling indicated that the edema in the
airway wall was mostly outside the smooth muscle and that the smooth
muscle shortening with histamine was similar with and without edema.
We conclude that a moderate degree of acute airway wall thickening
can lead to a potentiated constrictor response to histamine.
Received 12 December 1994; accepted in final form 26 May 1995.
APS Manuscript Number A1266-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.