Reflex control of breathing following inhalation of cigarette smoke in conscious dogs.
The acute ventilatory response to spontaneously inhaled cigarette smoke (750 ml, 10% concentration) was studied in 92 experiments on 6 awake resting dogs. Upon the first or second breath of smoke inhalation, either an apnea or an augmented breath was elicited consistently in each dog, and a hyperpnea occurred subsequently. Minute ventilation (VE) increased from a base line of 3.2 to a peak of 23.9 l/min at 8.3 s (mean values) after the smoke was completely inhaled and returned toward base line in 1-3 min. Cold blocking of both vagi (exteriorized in skin loops) eliminated the initial change in breathing pattern but did not significantly reduce the delayed hyperpnea. Denervation of carotid body chemoreceptors alone abolished 71.5% of the increase in VE induced by cigarette smoke. These results suggest that the apnea or augmented breath immediately following the smoke inhalation is mediated through vagal afferents, whereas the delayed hyperpnea results primarily from the stimulation of carotid body chemoreceptors, presumably by the absorbed nicotine.
D000818:Animals; D002245:Carbon Dioxide / Q000494:pharmacology; D002248:Carbon Monoxide / Q000494:pharmacology; D002344:Carotid Body / Q000502:physiology; D002628:Chemoreceptor Cells / Q000502:physiology; D003243:Consciousness; D003714:Denervation; D004285:Dogs; D009407:Nerve Block; D012018:Reflex / Q000187:drug effects*; D012119:Respiration / Q000187:drug effects*; D012907:Smoking; D013990:Tidal Volume; D014630:Vagus Nerve / Q000502:physiology
D002245:Carbon Dioxide; D002248:Carbon Monoxide