The interaction of chemo- and mechanoreceptor signals in the control of airway calibre.

The volume of an isolated tracheal segment and of the intrathoracic airways (intrathoracic portion of anatomical dead space) were measured during independent changes in ventilation minute volume and alveolar PCO2 and PO2, in order to assess the separate effects of chemoreceptor and mechanoreceptor signals upon airway calibre. The results were highly dependent upon initial airway tone, initial airway constriction favouring dilator responses and vice versa. Increasing alveolar PCO2 caused reflex airway constriction if ventilation was held constant. The magnitude of this response was reduced if ventilation was maintained at a high level and increased if it was held at a low level. Increasing ventilation caused reflex airway dilatation even if end tidal PCO2 was held constant. The size of the dilatation was reduced at high PCO2s and increased at low PCO2s. The interactions of the chemoreceptor and mechanoreceptor signals and of the effect of initial airway tone put a limit on airway dilatation during hyperventilation and particularly during hypercapnic hyperventilation. These mechanisms also limit the airway constriction following reductions in ventilation. They are consistent with the existence of an airway control system which adjusts airway calibre to minimise the work of breathing.