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A. Stransky, Magorzata Szereda-Przestaszewska and J. G. Widdicombe

1. The reflex action of stimulation of alveolar J-receptors and of airway epithelial irritant receptors has been investigated on laryngeal resistance to airflow and on laryngeal motoneurone discharge in cats and rabbits.

2. Resistance to airflow of the innervated larynx was measured (1) with the larynx isolated in situ with constant flow from the trachea to a pharyngeal opening; and (2) with the animal breathing through the larynx and the pharyngeal opening. With both methods resistance was determined from the relationship between translaryngeal pressure and airflow.

3. In control conditions the laryngeal resistance was about one tenth of total lung resistance.

4. I.V. injections of phenyl diguanide (to stimulate J-receptors) caused apnoea and complete closure of the larynx, followed by rapid shallow breathing with expiratory constrictions of the larynx. Expiratory laryngeal motoneurones were strongly stimulated.

5. The laryngeal responses to phenyl diguanide were nearly abolished by bilateral vagotomy in the chest (below the origin of the recurrent laryngeal nerves), and were absent on injection of the drug into the left atrium; the motoneurone responses were abolished by vagotomy and lessened by paralysis and artificial ventilation.

6. I.V. injections of histamine acid phosphate or inhalation of an aerosol of the drug in solution (to stimulate lung irritant receptors) caused tachypnoea and expiratory constrictions of the larynx, and increased discharges in expiratory laryngeal motoneurones.

7. The laryngeal responses to histamine were more than halved by bilateral intrathoracic vagotomy.

8. Phenyl diguanide and histamine increased the frequency of the discharge of inspiratory laryngeal motoneurones, but reduced the number of impulses per inspiratory phase. Laryngeal resistance in inspiration was usually increased.

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