Nasopharyngeal Reflexes: Integrative Analysis of Evoked Respiratory and Cardiovascular Effects

Summary Trigeminal afferents in the nasopharynx of unanaesthetized rabbits detect substances in the inspired air potentially damaging to the respiratory tree, and initiate reflex apnoea in expiration, bradycardia, a rise in mean arterial pressure and widespread reduction in blood flow and peripheral conductance. The apnoea is due to direct suppression of respiratory neurones by trigeminal activity activity maninly in bulbospinal regions, and the cardiovascular changes to direct trigeminal effects, to trigminal‐artrerial baroreceptor interactions, and to lung inflation‐arterial baroreceptor interactions in both suprabulbar and bulbospinal regions. Integration of trigeminal input occurs mainly at bulbospinal sites, where trigeminal ‐arterial baroreceptor‐ interactions are responsible for vagal motoneurone excitation, and direct trigeminal effects for excitation of mesenteric vasomotor neurones. Integration of the lung inflation input occurs at both suprabulbar and bulbospinal sites, lung inflation‐arterial baroreceptor Interactions at each site contributing to vagal excitation, but lung inflation‐arterial baroreceptor interactions only at suprabulbar sites causing excitation of mesenteric vasomotor neurones. The result of the increased vagal and sympathetic vasomotor activity is to lower profoundly blood flow in all soft tissue beds except the brain, for which a close to normal perfusion pressure is maintained. The peripheral effects act to reduce the rate of fall of circulating blood oxygen levels in the face of continuing apnoea. The asphyxial blood gas changes stimulate arterial chemoreceptors which contribute to the recommencement of respiration, and, if the environmental threat has dissipated, respiration continues and the cardiovascular effects subside.