MECHANISMS OF BRONCHIAL HYPERRESPONSIVENE SS - BRONCHIAL EDEMA, MECHANICAL AND VASCULAR FACTORS

Hindrance to gas flow in the bronchi is affected not only by airway sm ooth muscle tone but also by airway circulation. Congestion and oedema increase airway wall thickness and act in series with airway smooth m uscle contraction to reduce airway calibre, an effect which is more ma rked in small and intermediate bronchi. Many mediators, neuromediators , paracrine mediators produced by resident (epithelium) or migrant (in flammatory cells) cells share bronchomotor and vascular effects. In ad dition, contraction of airway smooth muscle and vascular phenomena are mechanically coupled. Contraction of airway smooth muscle facilitates vascular congestion and cedema because the diameter of the muscle rin g is more reduced than the external diameter of the airways. In additi on, a negative intrathoracic pressure, e.g. in asthma, increases the m echanical loading of both ventricles, thereby facilitating pulmonary a nd bronchial cedema. The effects of this mechanical coupling are enhan ced by airway inflammation that facilitates both vascular congestion a nd leakage. Stimuli such as exercise and hyperventilation cause airway vasodilatation which, in turn, facilitates and, possibly, triggers th e post-exercise asthma attack. Conversely, congestion and vasodilatati on may have a protective effect through an increase in the clearance o f bronchoconstrictor substances, or in reducing the amplitude of airwa y cooling and water loss in exercise-induced asthma. The relative role in bronchial hyperresponsiveness of airway smooth muscle contraction and vascular phenomena probably depends upon individual factors such a s, for instance, both intensity and nature of inflammation of the airw ay walls.