Document Detail


Mucociliary transport in porcine trachea: differential effects of inhibiting chloride and bicarbonate secretion.
MedLine Citation:
PMID:  23204069     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study was designed to assess the relative importance of Cl(-) and HCO(3)(-) secretion to mucociliary transport rate (MCT) in ex vivo porcine tracheas. MCT was measured in one group of tissues that was exposed to adventitial HCO(3)(-)-free solution while a parallel group was exposed to adventitial HCO(3)(-)-replete solution. After measurement of baseline MCT rates, acetylcholine (ACh) was added to stimulate submucosal gland mucous liquid secretion, and MCT rates were again measured. Before ACh addition, the mean MCT was higher in the HCO(3)(-)-free group (4.2 ± 0.9 mm/min) than in the HCO(3)(-)-replete group (2.3 ± 0.3 mm/min), but this difference was not statistically significant. ACh addition significantly increased MCT in both groups, but ACh-stimulated MCT was significantly lower in the HCO(3)(-)-free group (11.0 ± 1.5 mm/min) than in the HCO(3)(-)-replete group (17.0 ± 2.0 mm/min). A second series of experiments examined the effect on MCT of blocking Cl(-) secretion with 100 μM bumetanide. Before adding ACh, MCT in the bumetanide-treated group (1.0 ± 0.2 mm/min) was significantly lower than in the control group (3.8 ± 1.1 mm/min). ACh addition significantly increased MCT in both groups, but there was no significant difference between the bumetanide-treated group (21.4 ± 1.7 mm/min) and control group (19.5 ± 3.4 mm/min). These results indicate that ACh-stimulated MCT has greater dependence on HCO(3)(-) secretion, whereas the basal MCT rate has greater dependence on Cl(-) secretion.
Authors:
Jeffrey L Cooper; Paul M Quinton; Stephen T Ballard
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-11-30
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  304     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-04     Completed Date:  2013-03-26     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L184-90     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Animals
Bicarbonates / antagonists & inhibitors,  metabolism*
Bumetanide / pharmacology
Chlorides / antagonists & inhibitors,  metabolism*
Cholinergic Agonists / pharmacology
Mucociliary Clearance / drug effects*
Mucus / drug effects,  physiology
Organ Culture Techniques
Sodium Potassium Chloride Symporter Inhibitors / pharmacology
Swine
Trachea / drug effects*,  physiology
Grant Support
ID/Acronym/Agency:
R01HL-063302/HL/NHLBI NIH HHS; R01HL-84042/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Bicarbonates; 0/Chlorides; 0/Cholinergic Agonists; 0/Sodium Potassium Chloride Symporter Inhibitors; 0Y2S3XUQ5H/Bumetanide; N9YNS0M02X/Acetylcholine
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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