AN EFFERENT PATHWAY MEDIATING REFLEX TRACHEAL DILATION IN AWAKE DOGS

Lung inflation is known to produce reflex relaxation of tracheal smooth muscle (TSM) and dilation of the upper airway, but the specific efferent pathway involved is not established. TSM tone was examined in 4 trained awake dogs by measuring pressure changes in the water-filled cuff of an endotracheal tube that was inserted into the lower cervical trachea through a permanent tracheostomy. Under control conditions, sustained lung inflation with 1 l of air produced apnea (Hering-Breuer inflation reflex) and a decrease in cuff pressure (Pcuff) of 37.4 .+-. 12.0 (mean .+-. SD) cmH2O. .beta.-Adrenergic blockade with propranolol had no effect on either the apneic or TSM responses to lung inflation. Efferent parasympathetic blockade with atropine sulfate (1.2-2.4 mg) abolished TSM tone, which was then restored to control levels by a continuous i.v. infusion of serotonin [5-hydroxytryptamine] (14-28 .mu.g .cntdot. kg-1 .cntdot. min-1). Under these conditions, lung inflation still induced reflex apnea, but no longer relaxed TSM tone (mean decrease in Pcuff, 2.7 .+-. 1.4 cm H2O, P < 0.001). Reflex tracheal dilation in response to lung inflation is mediated by an efferent cholinergic (parasympathetic) pathway.