Journal article
Cigarette smoke inhibition of ion transport in canine tracheal epithelium
The Journal of clinical investigation, Vol.71(6), pp.1614-1623
06/1983
DOI: 10.1172/jci110917
PMCID: PMC370367
PMID: 6863537
Abstract
Inhalation of cigarette smoke is known to impair pulmonary mucociliary clearance. Active ion transport by airway epithelium plays an important role in maintaining effective mucociliary clearance by regulating the volume and composition of the airway secretions. To determine the effect of cigarette smoke on airway epithelial ion transport, the electrical properties and transepithelial Na and Cl fluxes were measured in canine tracheal epithelium. In vivo, the inhalation of the smoke from one cigarette acutely and reversibly decreased the electrical potential difference across the tracheal epithelium. In vitro, exposure of the mucosal surface of the epithelium to cigarette smoke decreased the short circuit current and transepithelial resistance. The decrease in short circuit current was due to an inhibition of the rate of Cl secretion with minimal effect on the rate of Na absorption. The effect of cigarette smoke was reversible, was not observed upon exposure of the submucosal surface to smoke, and was most pronounced when secretion was stimulated. The particulate phase of smoke was largely responsible for the inhibitory effect, since filtering the smoke minimized the effect. The effect of cigarette smoke was not prevented by addition of antioxidants to the bathing solutions, suggesting that the inhibition of Cl secretion cannot be entirely attributed to an oxidant mechanism. These results indicate that cigarette smoke acutely inhibits active ion transport by tracheal epithelium, both in vivo and in vitro. This effect may explain, in part, both the abnormal mucociliary clearance and the airway disease observed in cigarette smokers.
Details
- Title: Subtitle
- Cigarette smoke inhibition of ion transport in canine tracheal epithelium
- Creators
- M J Welsh
- Resource Type
- Journal article
- Publication Details
- The Journal of clinical investigation, Vol.71(6), pp.1614-1623
- Publisher
- American Society for Clinical Investigation
- DOI
- 10.1172/jci110917
- PMID
- 6863537
- PMCID
- PMC370367
- ISSN
- 0021-9738
- eISSN
- 1558-8238
- Grant note
- HL-14388 / NHLBI NIH HHS\r\nHL-07159 / NHLBI NIH HHS
- Language
- English
- Date published
- 06/1983
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Neurosurgery; Internal Medicine
- Record Identifier
- 9984020719202771
Metrics
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