Mechanism of Bronchoconstriction

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Abstract
Present studies in man and cats indicate that brief exposure to SO2 causes bronchoconstriction Vhich depends on intact motor parasympathetic pathways. The rapidity of response and its reversal suggests that changes in smooth muscle tone are the cause of the bronchoconstriction. SO2 stimulates sensory end organs arising in the trachea and bronchi. These fibers are believed to arise from the "cough" receptors ramifying between mucosal cells in the trachea and bronchi and having terminal filaments close to the ciliary plate of the epithelium. These are probably the receptors which transmit afferent impulses involved in the present experiments. The receptors occur in the upper as well as lower airways since lower airway constriction occurred when only the upper airway was exposed to SO2. The efferent limb of the broncho-constrictor reflex after inhalation of SO2 is in the vagus nerves. Other stimuli, including mechanical irritation of the larynx and inhalation of chemically inert dust aerosols19 reflexly increase resistance to airflow and stimulate coughing. The receptors responsible are thought to be cough receptors in the epithelium. The afferent and efferent pathways are in the vagus nerves. Thus, SO2 appears to act via pathways similar to other stimuli which stimulate cough receptors in producing reflex bronchoconstriction. Hypoxemia, hypercapnia, decreased arterial blood pressure, inhalation of inert dust particles, and mechanical irritation of the larynx constrict the airways reflexly while inflation of the lungs dilates the airways by initiating reflexes. Present studies give further evidence of reflex control of airways.