Trigeminally-mediated alteration of cardiorespiratory rhythms during nasal application of carbon dioxide in the rat.

Stimulation of the upper respiratory tract with air-borne irritants can result in dramatic alterations of cardiorespiratory rhythms that include apnea, bradycardia and selective peripheral vasoconstriction. Since carbon dioxide can stimulate receptors in the nasal passages, we wanted to determine if this odorless gas can induce the same autonomic changes as air-borne irritants. Passing 100% carbon dioxide through the nasal passages of rats anesthetized with chloralose-urethane produced apnea, a vagally-mediated bradycardia and a sympathetically-mediated increase in mean arterial blood pressure. Application of atropine blocked the bradycardia without affecting respiratory or blood pressure changes, while injection of prazosin eliminated blood pressure responses but did not affect heart rate or apnea. There were no significant autonomic responses to nasal application of 10, 25 or 50% carbon dioxide. The responses were mediated through the trigeminal innervation of the nasal mucosa since they could be blocked when the anesthetic procaine was applied to the nasal cavity. We conclude that these cardiorespiratory responses are due to stimulation of trigeminal nociceptors located within the nasal mucosa.