In the first edition of his classic text, Osler (1) listed several theories concerning the cause of asthma, which included (7) spasm of the bronchial muscles,(2) swelling of the bronchial mucous membrane, and (5) inflammation of the smaller bronchioles. He pointed out the similarities between the changes that occurred in the nasal mucous membranes in an attack of hay fever and those found in bronchi in asthmatics. He suggested that the exudation from a hyperemic swollen bronchial mucosa could explain the hindrance to respiration. He thought that those changes could either be by direct irritation of the bronchial mucosa or be induced by reflexes following stimulation of the nasal mucosa and other sites.

The excessive airway narrowing that occurs in asthmatic subjects in relation to both specific and nonspecific stimuli seems to have been clearly understood by Osler. Since then, much has been written about the contribution of smooth muscle contraction and edema of the airway wall to the narrowing of the lumen. Much more has been written about the release of inflammatory mediators from mast cells and eosinophils and other cells within the airway tissue. Many of these mediators contribute to fluid exudative and cellular components of the inflammatory response, as well as to the smooth muscle contraction. The purpose of this article is to try to understand how changes in airway structure and airway smooth muscle contraction bring about airway narrowing.