In normal airway defence and especially in asthma, mediators released from inflammatory cells will directly affect the walls of the abundant airway microvessels, making them much more permeable to macromolecules. Through large gaps between actively separated (contracted?) endothelial cells of venules of the tracheobronchial circulation, there is a bulk flow of proteinaceous plasma. The plasma exudate is distributed in the airway wall and it readily passes across an inflamed mucosa into the airway lumen. Plasma in the airway wall causes oedema, which may result in hyperresponsiveness and epithelial shedding. In the lumen its effects are formation of mucus plugs and inhibition of mucociliary transport, and its potent mediators such as the protein products of the kinin, complement, and clotting systems are released. Thus plasma exudation may operate in several aspects of asthmatic diathesis. By positive feedback mechanisms and recruitment and conditioning of inflammatory cells plasma exudate may amplify the inflammatory process.