Am. J. Respir. Cell Mol. Biol., Vol 11, No. 6, 12 1994, 724-732.
Dry air-induced mucosal cell injury and bronchovascular leakage in canine peripheral airways
AN Freed, C Omori, BH Schofield and W Mitzner
Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205.
The purpose of this study was to examine the relationship between
hyperpnea-induced mucosal injury, bronchovascular hyperpermeability, and
airway reactivity. Hyperpnea-induced bronchoconstriction was assessed by
measuring peripheral airway resistance (Rp) in anesthetized mechanically
ventilated male mongrel dogs. Either colloidal carbon or monastral blue was
used to localize bronchovascular leakage after a 5- min exposure to either
a 1000 ml/min dry, 2000 ml/min wet, or 2000 ml/min dry air challenge.
Morphometric analyses of cross-sectioned bronchi revealed that hyperpnea
with dry air stimulated goblet cell degranulation, damaged the bronchial
mucosa, and increased bronchovascular permeability. Exposure to only a 2000
ml/min dry air challenge produced marked mucosal injury when compared with
control. Regardless of treatment, bronchial vessels lying below normal
mucosa characterized by goblet/ciliated cell (G/C) ratios > or = 0.3 did
not leak. A G/C transition zone between 0 and 0.3 separated normal from
damaged mucosa. Within this zone, vascular permeability was inversely
correlated with G/C ratio. In addition, airflow-induced changes in Rp were
inversely related to G/C ratio and positively correlated with
bronchovascular leakage. Although these correlations are consistent with
the speculation that bronchovascular leakage and edema formation are
responsible for the dry air-induced changes in Rp, it is equally plausible
that bronchovascular leakage is not the cause of but occurs in concert with
airway narrowing to protect cells in the bronchial mucosa from excessive
losses of heat and water.
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Copyright © 1994 American Thoracic Society.
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