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J Appl Physiol (December 14, 2001). doi:10.1152/japplphysiol.00645.2001
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Articles in PresS, published online ahead of print December 14, 2001
J Appl Physiol, 10.1152/jap.00645.2001
Submitted on June 25, 2001
Accepted on December 10, 2001

An estimate of the subepithelial hydrostatic pressure that drives inflammatory transudate into the airway lumen

Vladimir B Serikov1, Yang J Jang1, and Jonathan H Widdicombe1*

1 Human physiology, University of California Davis, Davis, CA, USA

* To whom correspondence should be addressed. E-mail: vserikov{at}chori.org.

Inflammatory diseases of the upper respiratory tract are characterized by flow of plasma filtrate across the epithelium into the airway lumen ("transudation"). Elsewhere, we have proposed that extravasation from microvessels causes edema. This is associated with elevated subepithelial hydrostatic pressure that drives transudation. To test this hypothesis, we have attempted to block transudation by elevating luminal hydrostatic pressure. We measured the appearance of plasma markers into the lumen of an isolated perfused segment of trachea in vivo and found that stimulation of one vagal nerve caused a rapid (t1/2 ~ 5 min) and non-selective increase in the flow of markers from blood to airway lumen. Leukocyte migration also caused transudation that developed much more slowly (t1/2 = 2-3h). In both cases transudation was blocked by application of luminal hydrostatic pressures. The critical luminal pressure needed to block vagally-induced transudation was ~4.5 cm H2O and to block epithelial transudation induced by leukocyte traffic it was 3 cm H2O, and we conclude that these are the subepithelial pressure that drive inflammatory transudation into the airway lumen.




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