The role of microvascular permeability in the pathogenesis of asthma

Abstract

Proposed mediators of asthma act on specific pulmonary target tissues including the tracheobronchial microvasculature. Inflammatory extravasation of protein-rich plasma is obviously due to active mediator-induced formation of gaps between endothelial cells in the post-capillary venules of systemic microvessels. Because of this macromolecular permeability plasma exudate may accumulate interstitially and generate airway submucosal and mucosal oedema. The exudate apparently also passes into the airways lumen and has been suggested to affect the function and the attachment of the ciliated epithelial lining. The microvascular permeability to macromolecules is subject to specific physiological and pharmacological control. Both the mucosal (epithelial) and the microvascular barrier may exhibit an increased permeability in asthma, but must be considered two separate elements of the inflamed airway.