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Disruptive effects of Anion Secretion Inhibitors on Airway Mucus Morphology in Isolated Perfused Pig Lung
Author(s) -
Trout Laura,
Townsley Mary I.,
Bowden Amy L.,
Ballard Stephen T.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.035923
Subject(s) - mucus , mucin , secretion , bethanechol , lung , cystic fibrosis , submucosal glands , medicine , endocrinology , airway , bumetanide , biology , chemistry , ion transporter , biochemistry , anesthesia , receptor , ecology , muscarinic acetylcholine receptor , membrane
Since anion secretion inhibitors reproduce important aspects of cystic fibrosis (CF) lung disease, the effects of these antagonists on airway mucus morphology were assessed in isolated perfused pig lungs. Maximal inhibitory concentrations of bumetanide and dimethylamiloride, which respectively block Cl − and HCO 3 − secretion in porcine airways, induced the formation of dense ‘plastered’ mucus on the airway surface, depletion of periciliary fluid and collapse of cilia. This effect was more pronounced when lungs were also exposed to bethanechol to stimulate submucosal gland secretion, when plastered mucus covered > 98% of the airway surface. Bethanechol also reduced gland duct mucin content in the absence, but not presence, of the anion secretion inhibitors. Anion secretion inhibitors did not induce measurable increases in goblet cell degranulation. We conclude that inhibition of anion and liquid secretion in porcine lungs disrupts the normal morphology of airway surface mucus, providing further evidence that impaired anion secretion alone could account for critical aspects of CF lung disease.