Airway vasculature after mycoplasma infection: chronic leakiness and selective
hypersensitivity to substance P.
Kwan, Marilyn L., Antonio D. Gómez, Peter Baluk, Hiroya Hashizume, and Donald M.
McDonald.
Cardiovascular Research Institute and Department of Anatomy, University of
California, San Francisco, California 94143
APStracts 7:0256L, 2000.
Angiogenesis and microvascular remodeling are features of chronic airway inflammation
caused by Mycoplasma pulmonis infection in rats. As airway blood vessels undergo
remodeling, they become unusually sensitive to substance P-induced plasma leakage.
Here we determined whether the remodeled vessels are leaky under baseline conditions,
whether their heightened sensitivity is specific to substance P, and whether the leakage is
reversible. Four weeks after infection, the amount of baseline leakage of Evans blue in
the tracheal mucosa was two to five times the normal level. Gaps < 1 µm in diameter
were located between endothelial cells in some remodeled vessels. Substance P, but not
platelet-activating factor or 5-hydroxytryptamine, produced an exaggerated leakage
response. Inhalation of the ß2-adrenergic receptor agonist salmeterol reduced the leakage
by <60%. We conclude that the blood vessel remodeling after M. pulmonis infection is
associated with microvascular leakiness due, in part, to the formation of endothelial gaps.
This leakage is accompanied by an abnormal sensitivity to substance P but not to platelet-
activating factor or 5-hydroxytryptamine and can be reduced by ß2-agonists.
Received 25 January 2000; accepted in final form 10 August 2000
APS Manuscript Number L30-0.
Article publication pending Am J Physiol Lung Cell Mol Physiol
ISSN 1080-4757 Copyright 2000 The American Physiological Society.
Published in APStracts on 7 November 2000