Role of the Superior Pharyngeal Constrictor Muscle in Forced Breathing in Dogs

2000 ◽  
Vol 37 (2) ◽  
pp. 197-204 ◽  
Author(s):  
Zekai Yaman ◽  
Mikihiko Kogo ◽  
Hitomi Senoo ◽  
Seiji Iida ◽  
Shoichirou Ishii ◽  
...  

Objective Respiratory-related electromyographic (EMG) activity of the superior pharyngeal constrictor (SPC) muscle was analyzed during the early stage of forced breathing. Design Four adult dogs anesthetized with sodium pentobarbital were used. In the first part of the study, oral and nasal breathing tubes were placed into the respective cavities, and a tracheotomy tube was placed in the second part of the study. Two conditions, the presence (oral-nasal tube breathing) and absence (tracheotomy breathing) of airflow in the upper airway, were achieved in each dog. Following quiet breathing, animals were connected to a closed breathing system, first by an oral-nasal tube and then by a tracheotomy tube. We proposed to induce a forced breathing condition mechanically by using this system for 1 minute. We increased resistance to airflow during forced breathing by means of connecting tubes and a bag. Our aim was not to produce chemical drive but to produce a forced respiration by increasing the resistance to airflow. Tidal volume, breathing frequency, minute volume, chest wall movement, and EMG activity of the SPC muscle were measured and analyzed. Results During quiet breathing through an oral-nasal or tracheotomy tube, low-amplitude EMG activity of the SPC muscle corresponding to the expiratory cycle of the respiration was observed. In both study conditions, phasic expiratory EMG activity increased immediately after the advent of the breathing from the closed system. Tidal volumes and frequencies also increased rapidly during forced breathing. Conclusions An increase in the resistance to airflow increased the activity of the SPC muscle. This augmented respiratory activity probably assists the patency of the upper airway. The augmented respiratory activity was independent of the local reflex pathways. Respiratory-related activity of the SPC muscle may help dilate and stiffen the pharyngeal airway, promoting airway patency.

1986 ◽  
Vol 61 (4) ◽  
pp. 1523-1533 ◽  
Author(s):  
J. L. Roberts ◽  
W. R. Reed ◽  
O. P. Mathew ◽  
B. T. Thach

The genioglossus (GG) muscle activity of four infants with micrognathia and obstructive sleep apnea was recorded to assess the role of this tongue muscle in upper airway maintenance. Respiratory air flow, esophageal pressure, and intramuscular GG electromyograms (EMG) were recorded during wakefulness and sleep. Both tonic and phasic inspiratory GG-EMG activity was recorded in each of the infants. On occasion, no phasic GG activity could be recorded; these silent periods were unassociated with respiratory embarrassment. GG activity increased during sigh breaths. GG activity also increased when the infants spontaneously changed from oral to nasal breathing and, in two infants, with neck flexion associated with complete upper airway obstruction, suggesting that GG-EMG activity is influenced by sudden changes in upper airway resistance. During sleep, the GG-EMG activity significantly increased with 5% CO2 breathing (P less than or equal to 0.001). With nasal airway occlusion during sleep, the GG-EMG activity increased with the first occluded breath and progressively increased during the subsequent occluded breaths, indicating mechanoreceptor and suggesting chemoreceptor modulation. During nasal occlusion trials, there was a progressive increase in phasic inspiratory activity of the GG-EMG that was greater than that of the diaphragm activity (as reflected by esophageal pressure excursions). When pharyngeal airway closure occurred during a nasal occlusion trial, the negative pressure at which the pharyngeal airway closed (upper airway closing pressure) correlated with the GG-EMG activity at the time of closure, suggesting that the GG muscle contributes to maintaining pharyngeal airway patency in the micrognathic infant.


2016 ◽  
Vol 120 (7) ◽  
pp. 758-765 ◽  
Author(s):  
Mingshu Cai ◽  
Elizabeth C. Brown ◽  
Alice Hatt ◽  
Shaokoon Cheng ◽  
Lynne E. Bilston

Head and jaw position influence upper airway patency and electromyographic (EMG) activity of the main upper airway dilator muscle, the genioglossus. However, it is not known whether changes in genioglossus EMG activity translate into altered muscle movement during respiration. The aim of this study was to determine the influence of head and jaw position on dilatory motion of the genioglossus in healthy adult men during quiet breathing by measuring the displacement of the posterior tongue in six positions—neutral, head extension, head rotation, head flexion, mouth opening, and mandibular advancement. Respiratory-related motion of the genioglossus was imaged with spatial modulation of magnetization (SPAMM) in 12 awake male participants. Tissue displacement was quantified with harmonic phase (HARP) analysis. The genioglossus moved anteriorly beginning immediately before or during inspiration, and there was greater movement in the oropharynx than in the velopharynx in all positions. Anterior displacements of the oropharyngeal tongue varied between neutral head position (0.81 ± 0.41 mm), head flexion (0.62 ± 0.45 mm), extension (0.39 ± 0.19 mm), axial rotation (0.39 ± 0.2 mm), mouth open (1.24 ± 0.72 mm), and mandibular advancement (1.08 ± 0.65 mm). Anteroposterior displacement increased in the mouth-open position and decreased in the rotated position relative to cross-sectional area (CSA) ( P = 0.002 and 0.02, respectively), but CSA did not independently predict anteroposterior movement overall ( P = 0.057). The findings of this study suggest that head position influences airway dilation during inspiration and may contribute to variation in airway patency in different head positions.


1982 ◽  
Vol 52 (2) ◽  
pp. 438-444 ◽  
Author(s):  
O. P. Mathew ◽  
Y. K. Abu-Osba ◽  
B. T. Thach

The effects of change in pharyngeal airway pressure on electromyographic (EMG) activity of a pharyngeal dilating muscle (genioglossus) were investigated in 20 anesthetized rabbits. In vagotomized animals, upper airway loading maneuvers (nasal occlusion) increased the peak inspiratory activity of the genioglossus (GG) muscle on the first occluded breath. In contrast, “unloading” maneuvers (switching from nose to tracheostomy breathing) decreased GG activity. To further characterize the GG response, sustained pressure changes were produced within the isolated upper airway. Negative pressure increased GG activity; positive pressure decreased it. A poststimulus effect consisting of increased GG activity compared with control was seen following both negative- and positive-pressure stimuli. Cyclical pressure changes applied to the isolated upper airway increased the GG activity. These observations indicate the presence of reflex pathways that regulate GG muscle activity in response to upper airway pressure loads. This reflex system appears to play a role in regulating GG activity during tidal breathing and could be important in ensuring pharyngeal airway patency.


1999 ◽  
Vol 86 (1) ◽  
pp. 411-417 ◽  
Author(s):  
Samuel T. Kuna ◽  
Christi R. Vanoye

The mechanical effects of pharyngeal constrictor (PC) muscle activation on pharyngeal airway function were determined in 20 decerebrate, tracheotomized cats. In 10 cats, a high-compliance balloon attached to a pressure transducer was partially inflated to just occlude the pharyngeal airway. During progressive hyperoxic hypercapnia, changes in pharyngeal balloon pressure were directly related to phasic expiratory hyopharyngeus (middle PC) activity. In two separate protocols in 10 additional cats, the following measurements were obtained with and without bilateral electrical stimulation (0.2-ms duration, threshold voltage) of the distal cut end of the vagus nerve’s pharyngeal branch supplying PC motor output: 1) pressure-volume relationships in an isolated, sealed upper airway at a stimulation frequency of 30 Hz and 2) rostrally directed axial force over a stimulation frequency range of 0–40 Hz. Airway compliance determined from the pressure-volume relationships decreased with PC stimulation at and below resting airway volume. Compared with the unstimulated condition, PC stimulation increased airway pressure at airway volumes at and above resting volume. This constrictor effect progressively diminished as airway volume was brought below resting volume. At relatively low airway volumes below resting volume, PC stimulation decreased airway pressure compared with that without stimulation. PC stimulation generated a rostrally directed axial force that was directly related to stimulation frequency. The results indicate that PC activation stiffens the pharyngeal airway, exerting both radial and axial effects. The radial effects are dependent on airway volume: constriction of the airway at relatively high airway volumes, and dilation of the airway at relatively low airway volumes. The results imply that, under certain conditions, PC muscle activation may promote pharyngeal airway patency.


2009 ◽  
Vol 106 (3) ◽  
pp. 887-892 ◽  
Author(s):  
Kristina Kairaitis ◽  
Lauren Howitt ◽  
John R. Wheatley ◽  
Terence C. Amis

Lateral pharyngeal fat pad compression of the upper airway (UA) wall is thought to influence UA size in patients with obstructive sleep apnea. We examined interactions between acute mass/volume loading of the UA extra-luminal tissue space and UA patency. We studied 12 supine, anesthetized, spontaneously breathing, head position-controlled (50°), New Zealand White rabbits. Submucosal extraluminal tissue pressures (ETP) in the anterolateral (ETPlat) and anterior (ETPant) pharyngeal wall were monitored with surgically inserted pressure transducer-tipped catheters (Millar). Tracheal pressure (Ptr) and airflow (V̇) were measured via a pneumotachograph and pressure transducer inserted in series into the intact trachea, with hypopharyngeal cross-sectional area (CSA) measured via computed tomography, while graded saline inflation (0–1.5ml) of a compliant tissue expander balloon in the anterolateral subcutaneous tissue was performed. Inspiratory UA resistance (Rua) at 20 ml/s was calculated from a power function fitted to Ptr vs. V̇ data. Graded expansion of the anterolateral balloon increased ETPlat from 2.3 ± 0.5 cmH2O ( n = 11, mean ± SEM) to 5.0 ± 1.1 cmH2O at 1.5-ml inflation ( P < 0.05; ANOVA). However, ETPant was unchanged from 0.5 ± 0.5 cmH2O ( n = 9; P = 0.17). Concurrently, Rua increased to 119 ± 4.2% of baseline value ( n = 12; P < 0.001) associated with a significant reduction in CSA between 10 and 70% of airway length to a minimum of 82.2 ± 4.4% of baseline CSA at 40% of airway length ( P < 0.05). We conclude that anterolateral loading of the upper airway extraluminal tissue space decreases upper airway patency via an increase in ETPlat, but not ETPant. Lateral pharyngeal fat pad size may influence UA patency via increased tissue volume and pressure causing UA wall compression.


2019 ◽  
Vol 127 (5) ◽  
pp. 1307-1316
Author(s):  
Joshua Tong ◽  
Lauriane Jugé ◽  
Peter GR Burke ◽  
Fiona Knapman ◽  
Danny J Eckert ◽  
...  

Tracheal displacement is thought to be the primary mechanism by which changes in lung volume influence upper airway patency. Caudal tracheal displacement during inspiration may help preserve the integrity of the upper airway in response to increasing negative airway pressure by stretching and stiffening pharyngeal tissues. However, tracheal displacement has not been previously quantified in obstructive sleep apnea (OSA). Accordingly, we aimed to measure tracheal displacements in awake individuals with and without OSA. The upper head and neck of 34 participants [apnea-hypopnea index (AHI) = 2–74 events/h] were imaged in the midsagittal plane using dynamic magnetic resonance imaging (MRI) during supine awake quiet breathing. MRI data were analyzed to identify peak tracheal displacement and its timing relative to inspiration. Epiglottic pressure was measured separately for a subset of participants ( n = 30) during similar experimental conditions. Nadir epiglottic pressure and its timing relative to inspiration were quantified. Peak tracheal displacement ranged from 1.0–9.6 mm, with a median (25th–75th percentile) of 2.3 (1.7–3.5) mm, and occurred at 89 (78–99)% of inspiratory time. Peak tracheal displacement increased with increasing OSA severity (AHI) ( R2 = 0.28, P = 0.013) and increasing negative nadir epiglottic pressure ( R2 = 0.47, P = 0.023). Relative inspiratory timing of peak tracheal displacement also correlated with OSA severity, with peak displacement occurring earlier in inspiration with increasing AHI ( R2 = 0.36, P = 0.002). Tracheal displacements during quiet breathing are larger in individuals with more severe OSA and tend to reach peak displacement earlier in the inspiratory cycle. Increased tracheal displacement may contribute to maintenance of upper airway patency during wakefulness in OSA, particularly in those with severe disease. NEW & NOTEWORTHY Tracheal displacement is thought to play an important role in stabilizing the upper airway by stretching/stiffening the pharyngeal musculature. Using dynamic magnetic resonance imaging, this study shows that caudal tracheal displacement is more pronounced during inspiration in obstructive sleep apnea (OSA) compared with healthy individuals. Softer pharyngeal muscles and greater inspiratory forces in OSA may underpin greater tracheal excursion. These findings suggest that tracheal displacement may contribute to maintenance of pharyngeal patency during wakefulness in OSA.


PEDIATRICS ◽  
1981 ◽  
Vol 68 (6) ◽  
pp. 796-801
Author(s):  
Yousef K. Abu-Osba ◽  
Oommen P. Mathew ◽  
Bradley T. Thach

A series of experiments was performed in rabbits to investigate the effects of airway sensory stimuli on upper airway patency. Pharyngeal airway closure was observed in rabbits breathing through a tracheostomy tube; pharyngeal patency was rapidly restored either by closing the tracheostomy tube, which forced the animals to resume nasal breathing, or by creating cyclical pressure changes in the nose and pharynx to stimulate respiratory tidal airflow. This airway opening effect of pressure fluctuations was eliminated by topical anesthesia of the airway mucosa, an observation suggesting that sensory stimulation from pressure change is needed for airway patency. The observation that dead animals have a patent pharyngeal airway that is resistant to collapse from negative intraluminal pressure, whereas animals breathing via a tracheostomy have a readily collapsible airway that is closed at zero transmural pressure, suggests that airway-constricting muscles close the airway when the animals breathe via the tracheostomy. Loss of electromyographic activity from airway-dilating muscles (genioglossus) was observed during tracheostomal breathing and was restored by cyclical pressure changes applied to the upper airway lumen, an observation further supporting the concept that airway reflexes responding to pressure regulate the activity of airway-dilating and airway-constricting muscles. Topical anesthesia of the upper airway mucous membrane, which eliminated these responses to pressure, was associated with an obstructed pharynegal airway and death from apparent asphyxia in either pentobarbital-anesthetized adult animals or young animals without general anesthetic. Death resulting from airway obstruction in this manner was associated with postmortem findings of sudden infant death syndrome (pulmonary edema and pleural petechiae) in the majority of animals.


SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Olga Dergacheva ◽  
Thomaz Fleury-Curado ◽  
Vsevolod Y Polotsky ◽  
Matthew Kay ◽  
Vivek Jain ◽  
...  

Abstract Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive sleep-related losses of upper airway patency that occur most frequently during rapid eye movement (REM) sleep. Hypoglossal motoneurons play a key role in regulating upper airway muscle tone and patency during sleep. REM sleep activates GABA and glycine neurons in the ventral medulla (VM) to induce cortical desynchronization and skeletal muscle atonia during REM sleep; however, the role of this brain region in modulating hypoglossal motor activity is unknown. We combined optogenetic and chemogenetic approaches with in-vitro and in-vivo electrophysiology, respectfully, in GAD2-Cre mice of both sexes to test the hypothesis that VM GABA/glycine neurons control the activity of hypoglossal motoneurons and tongue muscles. Here, we show that there is a pathway originating from GABA/glycine neurons in the VM that monosynaptically inhibits brainstem hypoglossal motoneurons innervating both tongue protruder genioglossus (GMNs) and retractor (RMNs) muscles. Optogenetic activation of ChR2-expressing fibers induced a greater postsynaptic inhibition in RMNs than in GMNs. In-vivo chemogenetic activation of VM GABA/glycine neurons produced an inhibitory effect on tongue electromyographic (EMG) activity, decreasing both the amplitude and duration of inspiratory-related EMG bursts without any change in respiratory rate. These results indicate that activation of GABA/glycine neurons from the VM inhibits tongue muscles via a direct pathway to both GMNs and RMNs. This inhibition may play a role in REM sleep associated upper airway obstructions that occur in patients with OSA.


1992 ◽  
Vol 73 (2) ◽  
pp. 584-590 ◽  
Author(s):  
J. C. Leiter ◽  
S. L. Knuth ◽  
D. Bartlett

We investigated the quantitative relationships among pharyngeal resistance (Rph), genioglossal electromyographic (EMGge) activity, nasal resistance (Rna), and airflow in 11 normal men aged 19–50 while they were awake. We made measurements with subjects seated with the head erect, seated with the head flexed forward approximately 40 degrees, and supine. Each subject wore a face mask connected to a pneumotachograph to measure airflow. After topical anesthesia of the nose, two catheters for measuring nasal and pharyngeal airway pressures were passed through one nostril: the nasal pressure catheter was positioned at the nasal choanae, and the pharyngeal pressure catheter was positioned just above the epiglottis. We measured EMGge activity with an intraoral surface electrode. The subjects breathed exclusively through the nose while inhaling room air or rebreathing CO2. We measured Rph, Rna, airflow, and EMGge activity at approximately 90-ms intervals throughout each inspiration. Rph was invariant as head position was changed. At any given head position, EMGge activity rose as airflow increased, and Rph remained constant. In contrast, Rna increased as airflow increased. Because Rph was constant, EMGge activity was not correlated with Rph, but EMGge was positively correlated with Rna and airflow. On the basis of the stability of Rph in the face of marked changes in collapsing forces, we conclude that the dynamic interplay of posture, head and jaw position, and upper airway muscle activity quite effectively maintains pharyngeal patency, and interactions among these factors are subtle and complex.


1984 ◽  
Vol 56 (2) ◽  
pp. 500-505 ◽  
Author(s):  
O. P. Mathew

Influence of upper airway negative-pressure change on the respiratory activity of various upper airway muscles was investigated in 13 anesthetized rabbits. Phasic inspiratory activity increased or appeared during virtually all negative-pressure trials in nasolabial, cricothyroid, and posterior cricoarytenoid muscles. No phasic inspiratory activity was seen in the sternothyroid (ST) and sternohyoid (SH) muscles before negative-pressure applications but appeared during 80% of trials in ST and 62% of trials in SH. During maintained negative pressure, a gradual decline in activity was often observed in the nasolabial and laryngeal muscles, whereas a rapid decline in activity was seen in the cervical strap muscles. Reflex effects of negative pressure was markedly reduced or abolished by sectioning the internal branch of the superior laryngeal nerve bilaterally. Reflex augmentation of upper airway muscle activity reported here may have functional significance in the maintenance of upper airway patency. It could prevent upper airway collapse when negative pressure swings in the upper airway increase or facilitate recovery when large negative pressure swings are produced by obstructed inspiratory efforts.


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