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1 Department of Anesthesiology
and Critical Care Medicine,
2 Department of Radiology,
3 Division of Physiology,
Received 6 January 1997; accepted in final form 17 April 1997.
Brown, Robert H., Wayne Mitzner, and Elizabeth M. Wagner.
Interaction between airway edema and lung inflation on
responsiveness of individual airways in vivo. J. Appl.
Physiol. 83(2): 366-370, 1997.
bradykinin; high-resolution computed tomography; hyper-
responsiveness; hyperreactivity; methacholine
Inflammatory
changes and airway wall thickening are suggested to cause increased
airway responsiveness in patients with asthma. In five
sheep, the dose-response relationships of individual airways were
measured at different lung volumes to methacholine (MCh) before and
after wall thickening caused by the inflammatory mediator bradykinin
via the bronchial artery. At 4 cmH2O transpulmonary pressure
(Ptp), 5 µg/ml MCh constricted the airways to a maximum of 18 ± 3%. At 30 cmH2O Ptp, MCh resulted
in less constriction (to 31 ± 5%). Bradykinin increased airway
wall area at 4 and 30 cmH2O Ptp
(159 ± 6 and 152 ± 4%, respectively;
P < 0.0001). At 4 cmH2O Ptp, bradykinin decreased
airway luminal area (13 ± 2%; P < 0.01), and the dose-response curve was significantly lower (P = 0.02). At 30 cmH2O, postbradykinin, the maximal
airway narrowing was not significantly different (26 ± 5%;
P = 0.76). Bradykinin produced substantial airway wall thickening and slight potentiation of
the MCh-induced airway constriction at low lung volume. At high lung volume, bradykinin increased wall thickness but had no effect
on the MCh-induced airway constriction. We conclude that inflammatory
fluid leakage in the airways cannot be a primary cause of airway
hyperresponsiveness.
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society
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