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.
The role of different central nervous regions in the reflex apnea, bradycardia, and mesenteric vasoconstriction evoked by nasopharyngeal stimulation with cigarette smoke was examined in unanesthetized shamoperated, thalamic, and pontine rabbits with intact and sectioned carotid sinus and aortic nerves (CS and AN). Apnea occurred in all preparations. In pontine animals with intact CS and AN, the heart rate response was reduced but not the mesenteric vasoconstriction. The role of suprabulbar and bulbospinal regions became more apparent when individual components of the input profile were examined in animals with controlled ventilation. The bradycardia and mesenteric vasoconstriction evoked by apnea without smoke, but not by smoke without apnea, were reduced in pontine animals. Prior section of the CS and AN attenuated the response in all neural preparations but to the least extent when cerebral hemispheres were intact. The data indicate that the respiratory reflex is predominantly integrated at bulbospinal sites, but the cardiovascular reflex is integrated at both bulbospinal and suprabulbar sites, or is integrated at bulbospinal and modulated from suprabulbar sites.
The contributions of different afferent pathways to the reflex apnoea in expiration, mild hypertension and marked bradycardia evoked in unanaesthetized rabbits by nasal inhalation of cigarette smoke, formaldehyde, ammonia and benzene vapour were defined according to a factorial experimental design. Animals were used with (1) trigeminal nerve ablation, (2) olfactory bulb ablation, (3) total and selective section of the carotid sinus and aortic nerves, and (4) combinations of the above lesions. Trigeminal afferents are the primary source of the respiratory and circulatory disturbance. Olfactory afferents cannot initiate the respiratory and circulatory disturbance but weakly potentiate the apnoea induced by trigeminal stimulation. Arterial baroreceptor mechanisms contribute to the evoked bradycardia. Arterial chemoreceptor mechanisms do not contribute to the circulatory effects, but act to terminate the induced apnoea.
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