Influence of upper airway pressure changes on genioglossus muscle respiratory activity

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.


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.


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.


1990 ◽  
Vol 68 (6) ◽  
pp. 2581-2587 ◽  
Author(s):  
J. C. Leiter ◽  
J. A. Daubenspeck

In anesthetized or decerebrate animals, negative pressure applied to the upper airway selectively activates the hypoglossal nerve compared with the phrenic nerve. Conversely, positive pressure reduces hypoglossal nerve activity out of proportion to any change in the phrenic neurogram. We have tested the hypothesis that analogous pressure changes applied to awake humans would selectively inhibit or activate genioglossal electromyographic (EMGge) activity relative to diaphragmatic electromyographic activity (EMGdi). We studied seven normal subjects in a head-out body plethysmograph. Pressure at the mouth was either atmospheric, +10 cmH2O, or -10 cmH2O, and lung volume was held constant by applying an identical pressure to the body surface. Thus the transmural pressure distorting the respiratory system was applied only to the upper airway. Subjects breathed CO2-enriched (2-3%) room air to stimulate phasic respiratory EMGge activity. We found that -10 cmH2O pressure applied selectively to the upper airway resulted in a 49% enhancement of peak-integrated EMGge activity, but EMGdi activity remained at control levels. Positive pressure did not result in any changes in EMGge or EMGdi activity. Neither pressure resulted in significant changes in the magnitude or pattern of ventilation. We conclude that reflex mechanisms maintaining upper airway patency are demonstrable in awake humans and probably have an important role in moment-to-moment modulation of upper airway muscle activity in normal awake humans.


1982 ◽  
Vol 52 (2) ◽  
pp. 445-450 ◽  
Author(s):  
O. P. Mathew ◽  
Y. K. Abu-Osba ◽  
B. T. Thach

The afferent pathway of an upper airway reflex in which genioglossus muscle electromyographic (GG EMG) activity is influenced by pharyngeal pressure changes was investigated in 20 anesthetized rabbits. We took advantage of the fact that the upper airway was separated into two compartments by pharyngeal closure occurring when the animals breathe through a tracheostomy. This allowed pressure to be delivered selectively either to the nose and nasopharynx or to the larynx and hypopharynx. Midcervical vagotomy did not eliminate the GG EMG response to pressure stimuli. On the other hand high cervical vagotomy or superior laryngeal nerve section eliminated the response in the laryngeal compartment, but not in the nasopharyngeal compartment. Topical anesthesia of the mucosa of the nose, pharynx, and larynx abolished the response in both compartments. Therefore we conclude that more than one afferent pathway exists for this upper airway pressure reflex; the primary afferent pathway from the laryngeal compartment is the superior laryngeal branch of the vagus nerve, whereas the primary afferent pathway for the nasopharynx is nonvagal. Trigeminal nerve, glossopharyngeal nerve, and/or nervus intermedius carry nonvagal afferents from the nasopharynx and nose. The topical anesthetic and nerve section studies suggest that superficial receptors mediate this response. The occurrence of swallowing in response to upper airway pressure changes and its elimination by topical anesthesia or superior mechanoreceptors may mediate both genioglossus respiratory responses and swallowing responses.


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.


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.


1984 ◽  
Vol 18 ◽  
pp. 397A-397A
Author(s):  
Oommen P Mathew ◽  
John T Fisher ◽  
Franca B Sant'Ambrogio ◽  
Giuseppe Sant'Ambrogio

2009 ◽  
Vol 106 (5) ◽  
pp. 1668-1673 ◽  
Author(s):  
Ron Oliven ◽  
Naveh Tov ◽  
Majed Odeh ◽  
Luis Gaitini ◽  
Uri Steinfeld ◽  
...  

Both mandibular advancement (MA) and stimulation of the genioglossus (GG) have been shown to improve upper airway patency, but neither one achieves the effect of continuous positive airway pressure (CPAP) treatment. In the present study we assessed the combined effect of MA and GG stimulation on the relaxed pharynx in patients with obstructive sleep apnea (OSA). We evaluated responses of upper airway pressure-flow relationships and endoscopically determined pharyngeal cross-sectional area to MA and electrical stimulation of the GG in 14 propofol-anesthetized OSA patients. Measurements were undertaken at multiple levels of CPAP, enabling calculation of the critical closing pressure (Pcrit), upstream resistance (Rus), and pharyngeal compliance. GG stimulation, MA, and the combination of both shifted the pressure:flow relationships toward higher flow levels, resulting in progressively lower Pcrit (from baseline of 2.9 ± 2.2 to 0.9 ± 2.5, −1.4 ± 2.9, and −4.2 ± 3.3 cmH2O, respectively), without significant change in Rus. ΔPcrit during GG stimulation was significantly larger during MA than under baseline conditions (−2.8 ± 1.4 vs. −2.0 ± 1.4 cmH2O, P = 0.011). Combining the effect of GG stimulation with MA lowered Pcrit below 0 in all patients and restored pharyngeal patency to a level that enabled flow above the hypopnea level in 10/14 of the patients. Velopharyngeal compliance was not affected by either manipulation. We conclude that the combined effect of MA and GG stimulation is additive and may act in synergy, preventing substantial flow limitation of the relaxed pharynx in most OSA patients.


SLEEP ◽  
2019 ◽  
Vol 42 (7) ◽  
Author(s):  
Amal M Osman ◽  
Jayne C Carberry ◽  
Peter G R Burke ◽  
Barbara Toson ◽  
Ronald R Grunstein ◽  
...  

AbstractStudy ObjectivesA collapsible or crowded pharyngeal airway is the main cause of obstructive sleep apnea (OSA). However, quantification of airway collapsibility during sleep (Pcrit) is not clinically feasible. The primary aim of this study was to compare upper airway collapsibility using a simple wakefulness test with Pcrit during sleep.MethodsParticipants with OSA were instrumented with a nasal mask, pneumotachograph and two pressure sensors, one at the choanae (PCHO), the other just above the epiglottis (PEPI). Approximately 60 brief (250 ms) pulses of negative airway pressure (~ –12 cmH2O at the mask) were delivered in early inspiration during wakefulness to measure the upper airway collapsibility index (UACI). Transient reductions in the continuous positive airway pressure (CPAP) holding pressure were then performed during sleep to determine Pcrit. In a subset of participants, the optimal number of replicate trials required to calculate the UACI was assessed.ResultsThe UACI (39 ± 24 mean ± SD; range = 0%–87%) and Pcrit (–0.11 ± 2.5; range: –4 to +5 cmH2O) were quantified in 34 middle-aged people (9 female) with varying OSA severity (apnea–hypopnea index range = 5–92 events/h). The UACI at a mask pressure of approximately –12 cmH2O positively correlated with Pcrit (r = 0.8; p < 0.001) and could be quantified reliably with as few as 10 replicate trials. The UACI performed well at discriminating individuals with subatmospheric Pcrit values [receiver operating characteristic curve analysis area under the curve = 0.9 (0.8–1), p < 0.001].ConclusionsThese findings indicate that a simple wakefulness test may be useful to estimate the extent of upper airway anatomical impairment during sleep in people with OSA to direct targeted non-CPAP therapies for OSA.


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