Influence of carotid chemoreceptors on the vagal reflex-induced tracheal constriction

In this study, the effects of carotid chemoreceptors on reflex tracheal constriction were investigated in anesthetized, paralyzed, and artificially ventilated mongrel dogs. Reflex tracheal constriction was measured as changes in the intratracheal pressure of an air-filled balloon introduced into the rostral side of the transected trachea. A hypoxic condition was produced by ventilating the dog with 12% O2-88% N2. The reflex tracheal constriction induced by histamine inhalation to the bronchial side was reduced by section of the bilateral sinus nerves. The hypoxic condition significantly potentiated the reflex tracheal constriction induced by histamine inhalation. The potentiated reflex tracheal constriction during hypoxia was abolished by section of the bilateral sinus nerves. The afferent electrical stimulation to the central cut end of the vagus nerve caused a reflex tracheal constriction. The reflex tracheal constriction was significantly potentiated by hypoxia, and the potentiating response was abolished by section of the bilateral sinus nerves. The infusion of NaCN into the bilateral carotid arteries significantly potentiated the reflex tracheal constriction. The NaCN-induced potentiating effect was abolished by section of the bilateral sinus nerves. These results suggest that hypoxia potentiates the vagal reflex-induced tracheal constriction and that the hypoxia-induced potentiating effects may be mediated by carotid chemoreceptors.