Dilating forces on the upper airway of anesthetized dogs

1985 ◽  
Vol 58 (2) ◽  
pp. 452-458 ◽  
Author(s):  
K. P. Strohl ◽  
J. M. Fouke
Keyword(s):  
Muscle Activation ◽  
Moving Average ◽  
Upper Airway ◽  
Pressure Change ◽  
Emg Activity ◽  
Lung Inflation ◽  
Anesthetized Dogs ◽  
Cervical Trachea ◽  
Pressure Changes ◽  
Spontaneously Breathing

We reasoned that in an isolated sealed upper airway a pressure change would be caused by a change in airway volume. In eight spontaneously breathing anesthetized dogs, we isolated the upper airway by transecting the cervical trachea and sealing it from the lung and from the atmosphere. Pressure changes in this isolated upper airway were studied in relation to respiratory phase as evidenced by alae nasi electromyographic (EMG) activation and tidal volume measured at the distal trachea. A fall in pressure, indicating airway dilation, occurred with each spontaneous respiratory effort. Like the moving average of the alae nasi EMG, the pressure drop reached a peak value early in inspiration, was inhibited by further lung inflation, and was absent during passive mechanical ventilation. End-expiratory tracheal occlusion or vagotomy prolonged and augmented EMG activity and also the inspiratory fall in upper airway pressure. Increased levels of CO2 increased the magnitude of change in pressure during inspiration. An inhibiting effect of lung inflation was present to an equal extent at low and high levels of chemical drive. We show that dilation of the airway is concurrent with upper airway muscle activation during early inspiration, that this dilation increases with increasing chemical drive, and that vagal reflexes during lung inflation inhibit this dilation during the latter half of inspiration.

An efferent pathway mediating reflex tracheal dilation in awake dogs

1984 ◽  
Vol 57 (2) ◽  
pp. 413-418 ◽  
Author(s):  
G. Bowes ◽  
E. J. Shakin ◽  
E. A. Phillipson ◽  
N. Zamel
Keyword(s):  
Cuff Pressure ◽  
Upper Airway ◽  
Atropine Sulfate ◽  
Adrenergic Blockade ◽  
Continuous Intravenous Infusion ◽  
Lung Inflation ◽  
Efferent Pathway ◽  
Cervical Trachea ◽  
Pressure Changes ◽  
Parasympathetic Pathway

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 has not been established. Therefore we examined TSM tone in four 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 liter 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 intravenous infusion of serotonin (14–28 micrograms X kg-1 X 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 cmH2O, P less than 0.001). The findings indicate that reflex tracheal dilation in response to lung inflation is mediated by an efferent cholinergic (parasympathetic) pathway.

Effect of Chemoreceptor and Pulmonary Receptor Stimulation on Dilator Nares EMG Activity in the Dog

1983 ◽  
Vol 91 (6) ◽  
pp. 648-652 ◽  
Author(s):  
Daniel J. Blum ◽  
Thomas V. McCaffrey
Keyword(s):  
Upper Airway ◽  
Emg Activity ◽  
Receptor Stimulation ◽  
Lung Inflation ◽  
Anesthetized Dogs ◽  
Inspiratory Activity ◽  
Upper Airway Muscles ◽  
The Relationship ◽  
Pulmonary Stretch Receptor ◽  
Stimulation Of

To define the relationship between central control of upper airway muscles and respiratory muscle function, the electromyographic responses of the dilator nares muscles to stimulation of chemoreceptors and pulmonary receptors were studied in six anesthetized dogs. Only at maximal levels of hypoxia was the inspiratory activity of the dilator nares significantly increased. Hypercapnic stimulation increased the inspiratory activity with each incremental increase in CO2. Pulmonary stretch receptor stimulation produced by lung inflation inhibited dilator nares activity. Pulmonary irritant receptor stimulation by intravenously administered histamine increased dilator nares activity, as did pulmonary J receptor stimulation by the intravenous administration of capsaicin.

Response of laryngeal mechanoreceptors to high-frequency pressure oscillation

1992 ◽  
Vol 73 (1) ◽  
pp. 219-223 ◽  
Author(s):  
S. Zhang ◽  
O. P. Mathew
Keyword(s):  
High Frequency ◽  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Pressure Oscillation ◽  
Pressure Change ◽  
Laryngeal Nerve ◽  
Similar Frequency ◽  
Afferent Fibers ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

High-frequency pressure oscillations (HFPO) in the upper airway induce arousal, activation of genioglossus muscle, and bronchoconstriction. The present study was designed to determine the response of superior laryngeal nerve afferent fibers to HFPO. In 10 anesthetized dogs spontaneously breathing through a tracheal cannula, the upper airway was converted to a closed system. The activity of thin bundles separated from the peripheral cut end of the superior laryngeal nerve was monitored. Of 104 mechanoreceptors identified, 87 were classified as respiratory modulated and 17 as non-respiratory modulated on the basis of their response to transmural pressure change and muscle activity. The responses of these fibers to HFPO of +/- 2.5 cmH2O at 10, 20, and 30 Hz were determined. Among the respiratory-modulated receptors, 86 of 87 increased their activity in response to HFPO. Of the 17 non-respiratory-modulated receptors, 12 receptors showing a random or tonic activity did not respond to HFPO, whereas the 5 that were silent during control condition responded exclusively to HFPO. Our results show that HFPO of similar frequency but much less magnitude than snoring is capable of activating the vast majority of laryngeal mechanoreceptors. Pressure-sensitive respiratory-modulated endings appear to mediate the arousal and genioglossal response, whereas non-respiratory-modulated receptors responding to HFPO presumably mediate the bronchoconstrictive response.

Pressure-volume behavior of the upper airway

1986 ◽  
Vol 61 (3) ◽  
pp. 912-918 ◽  
Author(s):  
J. M. Fouke ◽  
J. P. Teeter ◽  
K. P. Strohl
Keyword(s):  
Peak Pressure ◽  
Force Production ◽  
Upper Airway ◽  
Volume Relationship ◽  
Anesthetized Dogs ◽  
Cervical Trachea ◽  
Force Volume ◽  
Pressure Changes ◽  
Upper Airway Muscles ◽  
The Relationship

The study was performed to investigate the relationship between force generation and upper airway expansion during respiratory efforts by upper airway muscles. In 11 anesthetized dogs we isolated the upper airway (nasal, oral, pharyngeal, and laryngeal regions) by transecting the cervical trachea and sealing the nasal and oral openings. During spontaneous respiratory efforts the pressure within the sealed upper airway, used as an index of dilating force, decreased during inspiration. On alternate breaths the upper airway was opened to a pneumotachograph, and an increase in volume occurred, also during inspiration. Progressive hyperoxic hypercapnia produced by rebreathing increased the magnitude of change in pressure and volume. At any level of drive, peak pressure or volume occurred at the same point during inspiration. At any level of drive, volume and pressure changes increased with end-expiratory occlusion of the trachea. The force-volume relationship determined from measurements during rebreathing was compared with pressure-volume curves performed by passive inflation of the airway while the animal was apneic. The relationship during apnea was 1.06 +/- 0.55 (SD) ml/cmH2O, while the force-volume relationship from rebreathing trials was -1.09 +/- 0.45 ml/cmH2O. We conclude that there is a correspondence between force production and volume expansion in the upper airway during active respiratory efforts.

Thoracic influence on upper airway patency

1988 ◽  
Vol 65 (5) ◽  
pp. 2124-2131 ◽  
Author(s):  
W. B. Van de Graaff
Keyword(s):  
Muscle Activity ◽  
Upper Airway ◽  
Constant Flow ◽  
Airway Patency ◽  
Anesthetized Dogs ◽  
Measured Resistance ◽  
Flow Through ◽  
Phrenic Nerves ◽  
Tracheostomy Tubes ◽  
Spontaneously Breathing

Patency of the upper airway (UA) is usually considered to be maintained by the activity of muscles in the head and neck. These include cervical muscles that provide caudal traction on the UA. The thorax also applies caudal traction to the UA. To observe whether this thoracic traction can also improve UA patency, we measured resistance of the UA (RUA) during breathing in the presence and absence of UA muscle activity. Fifteen anesthetized dogs breathed through tracheostomy tubes. RUA was calculated from the pressure drop of a constant flow through the isolated UA. RUA decreased 31 +/- 5% (SEM) during inspiration. After hyperventilating seven of these dogs to apnea, we maximally stimulated the phrenic nerves to produce paced diaphragmatic breathing. Despite absence of UA muscle activity, RUA fell 51 +/- 11% during inspiration. Graded changes were produced by reduced stimulation. In six other dogs we denervated all UA muscles. RUA still fell 25 +/- 7% with inspiration in these spontaneously breathing animals. When all caudal ventrolateral cervical structures mechanically linking the thorax to the UA were severed, RUA increased and respiratory fluctuations ceased. These findings indicate that tonic and phasic forces generated by the thorax can improve UA patency. Inspiratory increases in UA patency cannot be attributed solely to activity of UA muscles.

Anatomic consequences of intrinsic tongue muscle activation

2006 ◽  
Vol 101 (5) ◽  
pp. 1377-1385 ◽  
Author(s):  
E. Fiona Bailey ◽  
Yu-Hsien Huang ◽  
Ralph F. Fregosi
Keyword(s):  
Electrical Stimulation ◽  
Muscle Activation ◽  
Critical Role ◽  
Upper Airway ◽  
Pressure Source ◽  
Airway Patency ◽  
Tongue Muscle ◽  
Airway Pressures ◽  
Tongue Muscles ◽  
Spontaneously Breathing

We recently showed respiratory-related coactivation of both extrinsic and intrinsic tongue muscles in the rat. Here, we test the hypothesis that intrinsic tongue muscles contribute importantly to changes in velopharyngeal airway volume. Spontaneously breathing anesthetized rats were placed in a MRI scanner. A catheter was placed in the hypopharynx and connected to a pressure source. Axial and sagittal images of the velopharyngeal airway were obtained, and the volume of each image was computed at airway pressures ranging from +5.0 to −5.0 cmH2O. We obtained images in the hypoglossal intact animal (i.e., coactivation of intrinsic and extrinsic tongue muscles) and after selective denervation of the intrinsic tongue muscles, with and without electrical stimulation. Denervation of the intrinsic tongue muscles reduced velopharyngeal airway volume at atmospheric and positive airway pressures. Electrical stimulation of the intact hypoglossal nerve increased velopharyngeal airway volume; however, when stimulation was repeated after selective denervation of the intrinsic tongue muscles, the increase in velopharyngeal airway volume was significantly attenuated. These findings support our working hypothesis that intrinsic tongue muscles play a critical role in modulating upper airway patency.

Posture effects on timing of abdominal muscle activity during stimulated ventilation

1999 ◽  
Vol 86 (6) ◽  
pp. 1994-2000 ◽  
Author(s):  
Tadashi Abe ◽  
Takumi Yamada ◽  
Tomoyuki Tomita ◽  
Paul A. Easton
Keyword(s):  
Muscle Activity ◽  
Muscle Activation ◽  
Moving Average ◽  
Abdominal Muscle ◽  
Transversus Abdominis ◽  
Emg Activity ◽  
Abdominal Muscles ◽  
External Oblique ◽  
End Tidal ◽  
Internal Oblique

In humans during stimulated ventilation, substantial abdominal muscle activity extends into the following inspiration as postexpiratory expiratory activity (PEEA) and commences again during late inspiration as preexpiratory expiratory activity (PREA). We hypothesized that the timing of PEEA and PREA would be changed systematically by posture. Fine-wire electrodes were inserted into the rectus abdominis, external oblique, internal oblique, and transversus abdominis in nine awake subjects. Airflow, end-tidal CO2, and moving average electromyogram (EMG) signals were recorded during resting and CO2-stimulated ventilation in both supine and standing postures. Phasic expiratory EMG activity (tidal EMG) of the four abdominal muscles at any level of CO2 stimulation was greater while standing. Abdominal muscle activities during inspiration, PEEA, and PREA, were observed with CO2stimulation, both supine and standing. Change in posture had a significant effect on intrabreath timing of expiratory muscle activation at any level of CO2stimulation. The transversus abdominis showed a significant increase in PEEA and a significant decrease in PREA while subjects were standing; similar changes were seen in the internal oblique. We conclude that changes in posture are associated with significant changes in phasic expiratory activity of the four abdominal muscles, with systematic changes in the timing of abdominal muscle activity during early and late inspiration.

scholarly journals Modulation of laryngeal and respiratory pump muscle activities with upper airway pressure and flow

2001 ◽  
Vol 91 (2) ◽  
pp. 897-904 ◽  
Author(s):  
M. H. Stella ◽  
S. J. England
Keyword(s):  
Negative Pressure ◽  
Muscle Activity ◽  
Upper Airway ◽  
Abdominal Muscle ◽  
Positive Pressure ◽  
Emg Activity ◽  
Posterior Cricoarytenoid ◽  
Spontaneously Breathing ◽  
Respiratory Muscle Activity ◽  
Stimulation Of

The hypothesis that upper airway (UA) pressure and flow modulate respiratory muscle activity in a respiratory phase-specific fashion was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. We generated negative pressure and inspiratory flow in phase with tracheal inspiration or positive pressure and expiratory flow in phase with tracheal expiration in the isolated UA. Stimulation of UA negative pressure receptors with body temperature air resulted in a 10–15% enhancement of phasic moving-time-averaged posterior cricoarytenoid electromyographic (EMG) activity above tonic levels obtained without pressure and flow in the UA (baseline). Stimulation of UA positive pressure receptors increased phasic moving-time-averaged thyroarytenoid EMG activity above tonic levels by 45% from baseline. The same enhancement of posterior cricoarytenoid or thyroarytenoid EMG activity was observed with the addition of flow receptor stimulation with room temperature air. Tidal volume and diaphragmatic and abdominal muscle activity were unaffected by UA flow and/or pressure, whereas respiratory timing was minimally affected. We conclude that laryngeal afferents, mainly from pressure receptors, are important in modulating the respiratory activity of laryngeal muscles.

Influence of upper airway sensory receptors on respiratory muscle activation in humans

1987 ◽  
Vol 63 (1) ◽  
pp. 368-374 ◽  
Author(s):  
S. Redline ◽  
K. P. Strohl
Keyword(s):  
Respiratory Muscle ◽  
Muscle Activation ◽  
Human Subjects ◽  
Upper Airway ◽  
Normal Subjects ◽  
Emg Activity ◽  
Sensory Receptors ◽  
Upper Airways ◽  
Before And After ◽  
Thoracic Muscles

We reasoned that neural information from upper airway (UA) sensory receptors could influence the relationship between UA and diaphragmatic neuromuscular responses to hypercapnia. In this study, the electromyographic (EMG) activities of the alae nasi (AN), genioglossus (GG), and chest wall (CW) or diaphragm (Di) to ventilatory loading were assessed in six laryngectomized, tracheostomized human subjects and in six subjects breathing with an intact UA before and after topical UA anesthesia. The EMG activities of the UA and thoracic muscles increased at similar rates with increasing hypercapnia in normal subjects, in subjects whose upper airways were anesthetized, and in laryngectomized subjects breathing with a cervical tracheostomy. Furthermore, in the laryngectomized subjects, respiratory muscle EMG activation increased with resistive inspiratory loading (15 cmH2O X l–1 X s) applied at the level of a cervical tracheostomy. At an average expired CO2 fraction of 7.0%, resistive loading resulted in a 93 +/- 26.3% (SE) increase in peak AN EMG activity, a 39 +/- 2.0% increase in peak GG EMG activity, and a 43.2 +/- 16.5% increase in peak CW (Di) EMG activity compared with control values. We conclude that the ventilatory responses of the UA and thoracic muscles to ventilatory loading are not substantially influenced by laryngectomy or UA anesthesia.

Soft palate muscle responses to negative upper airway pressure

1999 ◽  
Vol 86 (2) ◽  
pp. 523-530 ◽  
Author(s):  
T. C. Amis ◽  
N. O’Neill ◽  
J. R. Wheatley ◽  
T. van der Touw ◽  
E. di Somma ◽  
...  
Keyword(s):  
Soft Palate ◽  
Muscle Activity ◽  
Airway Pressure ◽  
Upper Airway ◽  
Emg Activity ◽  
Afferent Activity ◽  
Afferent Pathways ◽  
Levator Veli Palatini ◽  
Anesthetized Dogs ◽  
Muscle Responses

The afferent pathways and upper airway receptor locations involved in negative upper airway pressure (NUAP) augmentation of soft palate muscle activity have not been defined. We studied the electromyographic (EMG) response to NUAP for the palatinus, tensor veli palatini, and levator veli palatini muscles in 11 adult, supine, tracheostomized, anesthetized dogs. NUAP was applied to the nasal or laryngeal end of the isolated upper airway in six dogs and to four to six serial upper airway sites from the nasal cavity to the subglottis in five dogs. When NUAP was applied at the larynx, peak inspiratory EMG activity for the palatinus and tensor increased significantly ( P< 0.05) and plateaued at a NUAP of −10 cmH2O. Laryngeal NUAP failed to increase levator activity consistently. Nasal NUAP did not increase EMG activity for any muscle. Consistent NUAP reflex recruitment of soft palate muscle activity only occurred when the larynx was exposed to the stimulus and, furthermore, was abolished by bilateral section of the internal branches of the superior laryngeal nerves. We conclude that soft palate muscle activity may be selectively modulated by afferent activity originating in the laryngeal and hypopharyngeal airway.

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