PATHWAYS AND MECHANISMS INVOLVED IN NEURAL CONTROL OF LARYNGEAL SUBMUCOSAL GLAND SECRETION

The purpose of this study was to define the pathways and mechanisms in volved in the neural regulation of laryngeal mucosal gland functions. In anesthetized, paralyzed, and artificially ventilated dogs, the resp onses of laryngeal submucosal glands to stimulation of laryngeal mecha noreceptors and peripheral chemoreceptors were examined by measuring t he number of hillocks and volume of secreted fluid before and after ac tivation of sensory nerve endings. Compared with a control period, the number of hillocks and volume of secreted fluid significantly increas ed (P < 0.05) with mechanical stimulation of the vocal folds (n = 13) and with chemical activation of peripheral chemoreceptors by systemic administration of sodium cyanide (100 mu g/kg; n = 11). The reflex res ponses induced by vocal fold stimulation and activation of peripheral chemoreceptors were slightly decreased by interrupting transmission in the recurrent laryngeal nerves (P > 0.05) and were abolished by subse quent sectioning of superior laryngeal nerves or prior intravenous adm inistration of atropine methylnitrate (P < 0.05). In denervated animal s, topical application of nicotine on laryngeal epithelium caused sign ificant activation of submucosal glands (P < 0.05). We conclude that l aryngeal secretion can be significantly altered reflexly by stimulatio n of laryngeal sensory nerve endings and peripheral chemoreceptors, th at both superior and recurrent laryngeal nerves convey cholinergic out flow to laryngeal submucosal glands, and that nicotine acting locally activates laryngeal submucosal glands.