| Mucociliary transport in porcine trachea: differential effects of inhibiting chloride and bicarbonate secretion. | |
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MedLine Citation:
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PMID: 23204069 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Jeffrey L Cooper; Paul M Quinton; Stephen T Ballard |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2012-11-30 |
Journal Detail:
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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:
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Created Date: 2013-02-04 Completed Date: 2013-03-26 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L184-90 Citation Subset: IM |
Affiliation:
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Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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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:
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R01HL-063302/HL/NHLBI NIH HHS; R01HL-84042/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Bicarbonates; 0/Chlorides; 0/Cholinergic Agonists; 0/Sodium Potassium Chloride Symporter Inhibitors; 28395-03-1/Bumetanide; 51-84-3/Acetylcholine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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