Current theories of the pathophysiology of asthma.
Release of chemical mediators from sensitized mast cells is of established importance in allergic asthma and can account for most of the pathology and recognized changes in physiology. There is still uncertainty regarding specific modes of action of most of the drugs effective in the treatment of asthma. Changes in respiratory mucosal permeability induced directly or indirectly by viruses may initiate atopic sensitization in genetically predisposed subjects. Increased bronchial irritability accounts for much of the bronchoconstriction in both allergic and nonallergic asthma. Leukotrienes cause the bronchoconstriction in patients with aspirin sensitivity, but the factors that differentiate these patients from subjects who tolerate aspirin remain unknown. Asthmatics are characterized by a substantial increase in the number of alpha-adrenergic receptors and a more modest decrease in the number of beta-adrenergic receptors as well as increased sensitivity to cholinergic stimulation. Both mediator release and bronchial irritability may be important causes of exercise induced asthma.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000328:Adult; D000707:Anaphylaxis / Q000276:immunology; D001249:Asthma / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D001250:Asthma, Exercise-Induced / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000276:immunology; D002630:Chemotactic Factors / Q000276:immunology; D002648:Child; D006636:Histamine Release / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology
D000319:Adrenergic beta-Antagonists; D002630:Chemotactic Factors; D007073:Immunoglobulin E