Asthma results from variable and often sudden changes in airway smooth muscle tone. Allergy is not an essential component of the asthmatic response; however, mediator release plays an important role in the human asthmatic response. Histamine may act directly to cause bronchoconstriction by stimulating the H1-receptor on airway smooth muscle or indirectly by stimulation of afferent vagal fibers in airways. Histamine may also act locally on airways to augment cholinergic and, possibly, alpha-adrenergic constrictor effects, or to antagonize beta-adrenergic relaxation of airway smooth muscle. Cholinergic neural output promotes bronchoconstriction in non-atopic asthma, but parasympathetic reflexes are not a major component of human bronchial responses to inhaled allergen. The physiologic significance of the sympathetic nervous system in relaxing airway smooth muscle is incompletely defined. Recent studies suggest that direct sympathetic innervation of airways is relatively unimportant and that purinergic fibers may be the predominant inhibitory neurons in human airways. Investigations focusing on intracellular calcium metabolism in airway smooth muscle have implicated the adenyl cyclase-cyclic adenosine monophosphate system in the regulation of bronchomotor tone. Cyclic nucleotides may modulate but do not mediate respiratory muscle contraction, and their precise role in regulating bronchomotor tone remains uncertain.

Chronic bronchitis and emphysema (chronic obstructive pulmonary disease [COPD]) represent a major health problem in this country. Corticosteroids have provided an important advance in the management of bronchial asthma, but the role of these drugs in the therapy for COPD has not been defined clearly. To gain further insight into this problem, an overview of the pharmacologic properties and mechanisms of action of corticosteroids on the cellular systems of the lung and a critical analysis of the 17 studies evaluating the efficacy of therapy with corticosteroids in COPD were done. There are several theoretic reasons why corticosteroids might be useful in treating COPD; however the majority of studies have not demonstrated a positive effect, yet individual patients have attained marked improvement. An objectively monitored, finite trial of therapy with corticosteroids in the patient with COPD who has worsening symptoms is warranted, as the benefit is high in responsive individuals and the risk is low in nonresponders.

Abnormalities in small airways appear to be important in the evolution of chronic obstructive pulmonary disease. Patients with these pathologic lesions may have normal values for airway resistance and forced expiratory volume in one second. Two new tests, the closing volume (CV) and the dependence of maximal flow on density, are believed to be sensitive to abnormalities in the peripheral airways. The CV test detects an increased nonuniformity of changes in volume of pulmonary units. Reduced dependence of flow on density is believed to result from an increase in the peripheral component of the losses of driving pressure which determine maximal expiratory flow. Both tests differentiate smokers with normal conventional spirometric data from age-matched nonsmokers. Although this evidence suggests that these tests can be used to detect abnormalities in small airways, there is very little pathologic confirmation of this belief. The clinical significance of abnormalities in the results of either of these tests in an otherwise normal person has not yet been determined.