Cigarette smoke-induced bronchoconstriction in dogs: vagal and extravagal mechanisms.
We reassessed the severity of cigarette smoke-induced bronchoconstriction and the mechanisms involved in anesthetized dogs. To evaluate the severity of smoke-induced bronchoconstriction, we measured airway pressure and airflow resistance (Rrs, forced oscillation method). We studied the mechanisms in other dogs by measuring airway pressure, central airway smooth muscle tone in tracheal segments in situ, and respiratory center drive by monitoring phrenic motor nerve output, including the role of vagal and extravagal nerves vs. the role of blood-borne materials during inhalation of cigarette smoke. Rrs increased more than fourfold with smoke from one cigarette delivered in two tidal volumes. About half the airway response was due to local effects of smoke in the lungs. The remainder was due to stimulation of the respiratory center, which activated vagal motor efferents to the airway smooth muscle. Of this central stimulation, about half was due to blood-borne materials and the rest to vagal pulmonary afferents from the lungs. We conclude that inhalation of cigarette smoke in dogs causes severe bronchoconstriction which is mediated mainly by extravagal mechanisms.
D000403:Airway Resistance; D000818:Animals; D001980:Bronchi / Q000294:innervation*; D002799:Cholinergic Fibers / Q000502:physiology; D004285:Dogs; D007823:Laryngeal Nerves / Q000502:physiology; D008168:Lung / Q000294:innervation*; D009046:Motor Neurons / Q000502:physiology; D010791:Phrenic Nerve / Q000502:physiology; D012018:Reflex / Q000502:physiology; D012907:Smoking; D014132:Trachea / Q000294:innervation; D014630:Vagus Nerve / Q000502:physiology*