Afferent pathway(s) for pharyngeal dilator reflex to negative pressure in man: a study using upper airway anaesthesia.

Abstract

SUMMARY1. To determine the afferent pathways mediating pharyngeal dilator muscle activation in response to negative airway pressure in man, we recorded genioglossus electromyogram (EMG) activity (via intra-oral bipolar surface electrodes) in response to 500 ms duration pressure stimuli of -15 and -25 cmH20 in normal, conscious, supine subjects relaxed at end-expiration; responses were compared before and after upper airway anaesthesia.2. Six rectified and integrated EMG responses were bin averaged for pressure stimuli applied with the glottis open (GO) and closed (GC) and to the outside of the face only (controls). Response magnitude was quantified as the ratio of the EMG activity for an 80 ms post-stimulus period (before the subject's reaction time for tongue protrusion) to an 80 ms pre-stimulus period.3. In eight subjects, upper airway anaesthesia reduced the EMG responses with GC to a level indistinguishable from controls. After anaesthesia, responses with GO remained higher than those with GC.4. With GC, the mean EMG responses decreased by 43 % after selective anaesthesia of the nasal mucosa (trigeminal nerves) in two subjects, 32 % after selective anaesthesia of the laryngeal mucosa (superior laryngeal nerves) in six subjects and by 21 % after selective anaesthesia of the oropharyngeal mucosa (glossopharyngeal and lingual nerves) in four subjects.5. We conclude that upper airway afferents mediate pharyngeal dilator muscle activation in response to negative pressure with GC and that subglottal receptors cause the increased activation with GO. With GC, the trigeminal and superior laryngeal nerves mediate an important component of the responses with the glossopharyngeal nerves playing a less important role.

Smoking Induces Oropharyngeal Narrowing and Increases the Severity of Obstructive Sleep Apnea Syndrome

“…27,28 The afferent peripheral nerves in the airway mucosa respond to stimulation by fumes by secreting tachykinin, CGRP, and SP, which are required for neuroendocrinological inflammation. [29][30][31] We found that CGRP-positive staining was substantially more prevalent in the uvular mucosa of smokers compared to PGP 9.5 and SP staining. In particular, CGRP staining was increased in the uvular mucosa of patients exposed to smoking for > 10 PY.…”

Pathophysiology of obstructive sleep apnoea

“…Evidence suggests that these reflex mechanisms are pressure sensitive [112,[144][145][146], and interference with them could lead to an imbalance between intrapharyngeal pressure and the contraction of upper airway dilating muscles, resulting in obstructive apnoeas [3]. The importance of such protective reflexes is supported by the finding of fatal pharyngeal airway closure in rabbits, in which upper airway reflexes are abolished by topical anaesthesia [150].…”

“…Contributions from both supraglottic and subglottic receptors appear to be involved, and topical anaesthesia blocks the response when the glottis is closed [112]. This response is reduced during NREM sleep [154].…”

“…Breathing through a narrowed upper airway generates a greater suction pressure and, thus, greater collapsing force, and pharyngeal dilator muscles must, therefore, contract more forcefully to prevent upper airway obstruction. Progressive hypercapnia, hypoxia, asphyxia and negative pressure application all produce an augmenting drive to upper airway dilator muscles [107][108][109][110][111][112]. Defects in such upper airway muscle responses, or inco-ordination of upper airway and diaphragm activity, have each been proposed as factors predisposing to OSA [54,107,108,110,113,114].…”

“…Several reports indicate a role for upper airway reflex mechanisms in the maintenance of patency [111,112,[143][144][145][146][147][148][149]. Evidence suggests that these reflex mechanisms are pressure sensitive [112,[144][145][146], and interference with them could lead to an imbalance between intrapharyngeal pressure and the contraction of upper airway dilating muscles, resulting in obstructive apnoeas [3].…”