Airway vasculature after mycoplasma infection: chronic leakiness and selective hypersensitivity to substance P
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, th...
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Published in | American journal of physiology. Lung cellular and molecular physiology Vol. 280; no. 2; pp. 286 - L297 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.02.2001
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Subjects | |
Online Access | Get full text |
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Summary: | 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
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 2 -agonists.
angiogenesis; 2 -adrenoceptor agonists; endothelial
cells; Evans blue; inflammation; Mycoplasma pulmonis ; salmeterol; vascular permeability; Wistar rats; Fischer 344 rats |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1040-0605 1522-1504 |
DOI: | 10.1152/ajplung.2001.280.2.l286 |