| pubmed-article:2003691 | 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. | lld:pubmed |
