Role of trigeminal, olfactory, carotid sinus and aortic nerves in the respiratory and circulatory response to nasal inhalation of cigarette smoke and other irritants in the rabbit.

Abstract

SummaryThe 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.