Linked Life Data

2003691

Source:http://linkedlifedata.com/resource/pubmed/id/2003691

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 2
pubmed:dateCreated
1991-4-12
pubmed:abstractText
The release of mediators from inflammatory cells into the airway lumen can initiate a series of events leading to airway obstruction, particularly smooth muscle contraction and alteration of endothelial and epithelial permeability leading to mucosal edema and subsequent influx of liquid into the airway lumen. In this report we briefly review the effects of several inflammatory mediators, including eicosanoids, platelet-activating factor, and histamine, as well as the effects of plasma proteins and tachykinins that may be secondarily released because of the presence of inflammatory mediators on endothelial and epithelial permeability. We then consider physical mechanisms whereby the resulting airway luminal liquid could amplify the response of an airway previously constricted because of smooth muscle contraction. Specifically, liquid in the interstices between epithelial projections that are formed during muscular contraction could amplify the degree of luminal compromise by (1) further decreasing luminal cross-sectional area by occupying space, and (2) providing an additional source of inward recoil because of the surface tension of the air-liquid interface.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0003-0805
pubmed:author
pubmed:issnType
Print
pubmed:volume
143
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S52-4
pubmed:dateRevised
2011-10-25
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Airway luminal liquid. Sources and role as an amplifier of bronchoconstriction.
pubmed:affiliation
Department of Environmental Science and Physiology, Harvard School of Public Health, Boston, MA 02115.
pubmed:publicationType
Journal Article, Review