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Am J Physiol Lung Cell Mol Physiol 280: L286-L297, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 2, L286-L297, February 2001

Airway vasculature after mycoplasma infection: chronic leakiness and selective hypersensitivity to substance P

Marilyn L. Kwan, 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

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 beta 2-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 beta 2-agonists.

angiogenesis; beta 2-adrenoceptor agonists; endothelial cells; Evans blue; inflammation; Mycoplasma pulmonis; salmeterol; vascular permeability; Wistar rats; Fischer 344 rats


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