Hexamethonium aerosol prevents pulmonary reflexes induced by cigarette smoke in dogs.

The reflexogenic respiratory responses to spontaneous inhalation of cigarette smoke (500-750 ml, 12-20% concentration) were studied in chloralose anesthetized dogs before and after hexamethonium aerosol, a nicotinic receptor antagonist, was administered into the lungs. In 11 of 13 dogs studied, reproducible responses of either apnea (n = 9) or rapid shallow breathing (n = 2) were elicited immediately after the first or second breath of smoke inhalation: apneic duration reached 398 +/- 47% (mean +/- SEM) of the mean baseline expiratory duration. Pretreatment with hexamethonium aerosol (3-5 breaths, 10% concentration) completely abolished these immediate changes in breathing patterns, but did not significantly reduce the delayed hyperpnea induced by smoke inhalation. Hexamethonium aerosol alone did not cause any detectable systemic effects. To examine if a bronchoconstrictive effect of nicotine was involved, the response to cigarette smoke was also studied after bronchodilation was induced by isoproterenol aerosol (15 breaths, 0.5% concentration) in 6 of these dogs. However, neither immediate nor delayed responses to smoke inhalation was significantly affected. These results suggest that: (1) these immediate respiratory responses to smoke inhalation are elicited by a nicotine-induced stimulation of vagal sensory receptors in the lungs, and (2) bronchoconstriction is not responsible for causing these reflex effects.