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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: The Australian journal of experimental biology and medical science
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.