Tracheobronchial and laryngeal responses to hypercapnia, histamine and capsaicin in dogs.

In nine greyhound dogs, anaesthetized with chloralose-urethane, total lung resistance, volume of an isolated cervical tracheal segment and resistance of the isolated larynx were simultaneously measured. Three stimuli were tested: inhalation of a CO2-enriched gas mixture; histamine injected intravenously or administered by aerosol to stimulate primarily lung irritant receptors; and intravenous injection of capsaicin to stimulate primarily lung C-fibre receptors. The stimuli were applied in three successive conditions: neurally-intact animals; denervation of the right lung plus cold block of myelinated fibres in the left cervical vagus nerve; and further blockade of non-myelinated fibres in this nerve. Histamine and capsaicin increased lung and laryngeal resistances, and reduced tracheal volume, and the responses after denervation are consistent with the drugs acting by lung vagal reflexes. In neurally-intact animals, hypercapnia increased total lung resistance, decreased tracheal volume and lowered laryngeal resistance. After elimination of conduction in all myelinated fibres, CO2-induced changes in lung resistance and in tracheal volume were still present. However, the dilating effect of hypercapnia on the larynx diminished markedly. Elimination of all vagal pulmonary afferents abolished the residual laryngeal response to hypercapnia, lowered and delayed changes in tracheal volume and greatly reduced the increase in lung resistance. The results indicate that the laryngeal response to hypercapnia depends on vagal integrity, but the tracheobronchial constrictor effect of CO2 is less affected by vagal denervation.