Abstract

Publisher Summary This chapter discusses new approaches to bronchodilator and antiallergic drug therapy. Airway responsiveness in asthmatics is greatly increased, and this phenomenon, often referred to as airway or bronchial hyperreactivity, is a cardinal sign believed by many to be the primary pathogenetic event in the development of the disease. Several mechanisms have been proposed to explain the pathophysiology of bronchial hyperreactivity: (i) a decrease in baseline airway caliber, (ii) an elevation in the responsiveness of the bronchial smooth muscle, (iii) an imbalance in the autonomic nervous control of the airways, and (iv) a breakdown of airway defenses, allowing an increase in the accessibility of allergens or nonspecific stimuli to mast cells, sensory nerve endings, or bronchial smooth muscle. These mechanisms have been reviewed in detail by others, and it is apparent that airway hyperreactivity does not depend on just one factor. Therapeutic modulation of airway hyperreactivity is clearly highly desirable; however, most bronchodilator agents, perhaps with the exception of disodium cromoglycate (DSCG) and the corticosteroids do not appear to affect the underlying pathophysiology of hyperreactivity. The complexity of this phenomenon makes this goal exceedingly difficult to achieve at present.

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