[Bronchial hyperreactivity: state and perspective of drug intervention]

A decreased threshold of bronchial contractility under the influence of nonspecific and specific factors (bronchial hyperreactivity--BHR) is a disposing factor and precondition to the development of asthmatic disease. Probably the disturbance of the barrier function of the bronchial epithelium plays a central role in bronchial hyperreactivity. The release of phospholipid mediators from membrane phospholipids might be decisive for the establishment of bronchial hyperreactivity. This is documented, before all, by the decreasing effect of glucocorticosteroids upon the hyperreactivity since their pharmacologic efficacy is realized in first line by an inhibition of the release of arachidonic acid. We are arguing that an endogenously not compensated basical release of arachidonic acid and platelet activating factor is causally related to bronchial hyperreactivity. Prevention of asthma as well as therapy must aim at systematic reduction of bronchial hyperreactivity. Beside glucocorticosteroids and other inhibitors of phospholipase could prospectively be of therapeutic interest inhibitors of synthesis or antagonists of 5-lipoxygenase, of platelet activating factor, of leukotrienes or thromboxanes. There exist theoretical bases for practical measures of directed prevention of asthma in persons at risk. Their efficiency still awaits scientific evaluation.