Mechanisms of bronchoconstriction : a study of bronchial reactivity to SO₂ inhalation and to exercise in normal and atopic subjects and patients with asthma and chronic bronchitis

• Main Author: Tan, Wan-Cheng
• Published: University of Aberdeen 1981
• Subjects: 615.1; Respiratory medicine
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.349460

Bronchial hyperreactivity to non-allergic stimuli in allergic subjects can be measured by the increased bronchomotor response to the inhalation of controlled low concentrations of sulphur dioxide (5-20 ppm). This bronchomotor response is graded from the normal subjects and patients with chronic bronchitis who had the smallest response, to the atopic subjects with an intermediate response, to the asthmatic patient with the largest response. Allergic subjects could be distinguished from the non-allergic subjects by the intensity of this response, but it was not possible to consistently discriminate between asthmatic and non-asthmatic allergic subjects. Measurements of maximal flow at low lung volumes suggest that the site of action is in the intrathoracic as well as extrathoracic airways. The bronchomotor response to exercise, another non-allergic stimulus depends on the degree of airway cooling as determined by the temperature and humidity of the inspired air. The mechanism of action of irritant gas stimulation is multifactorial. The cholinergic reflex pathway has an important role as shown by the results of respiratory reflexes and efferent cholinergic blockade. However, this pathway seems to be relatively more important in allergic but non-asthmatic subjects than in patients with lower airway problems. Also, this mechanism is variable in patients with asthma. Another mechanism is that of mast cell release of mediators of anaphylaxis. Studies with a stabilizer of the mast cell membrane disodium cromoglycate, and an H₁ receptor antagonist clemastine, provide convincing indirect evidence of the importance of this mechanism in non-allergen triggered bronchoconstriction. However, in exercise-induced bronchoconstriction, a rise in plasma histamine is random and is probably the result of the stress of exercise and not the cause of bronchoconstriction. A definitive answer necessitates measurements of histamine in pulmonary venous blood, studies of the modulating effect of inhaled specific antagonists to histamine and other mediators on exercise-induced asthma.