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Figure 1.
Feline skull base showing relationship of tensor veli palatini to hamulus and palate. Wire electrodes are in the vertical portion of the isolated muscle belly.

Feline skull base showing relationship of tensor veli palatini to hamulus and palate. Wire electrodes are in the vertical portion of the isolated muscle belly.

Figure 2.
Bilateral tensor veli palatini stimulation. Data are means±SEMs. Maximal inspiratory airflow (V̇Imax) increased significantly with stimulation and was associated with a significant decrease in critical airway pressure (Pcrit) and an increase in nasal resistance (Rn).

Bilateral tensor veli palatini stimulation. Data are means±SEMs. Maximal inspiratory airflow (V̇Imax) increased significantly with stimulation and was associated with a significant decrease in critical airway pressure (Pcrit) and an increase in nasal resistance (Rn).

1.
Morrison  DLLaunois  SHIsono  SFeroah  TRWhitelaw  WARemmers  JE Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea. Am Rev Respir Dis. 1993;148606- 611Article
2.
Horner  RLShea  SAMcIvor  JGuz  A Pharyngeal size and shape during wakefulness and sleep in patients with obstructive sleep apnea. Q J Med. 1989;268719- 735
3.
Kogo  MKurimoto  TKoizumi  HNishio  JMatsuya  T Respiratory activities in relation to palatal muscle contraction. Cleft Palate Craniofac J. 1992;29174- 178Article
4.
Tangel  DJMezzanotte  WSWhite  DP Respiratory related control of palatoglossus and levator palatini muscle activity. J Appl Physiol. 1995;78680- 688
5.
Launois  SHRemsburg  SYang  WJWeiss  JW Relationship between velopharyngeal dimensions and palatal EMG during progressive hypercapnia. J Appl Physiol. 1996;80478- 485
6.
van der Touw  TO'Neill  NBrancatisano  AAmis  TWheatley  JREngel  LA Respiratory related activity of soft palate muscles: augmentation by negative upper airway pressure. J Appl Physiol. 1994;6424- 432
7.
Wheatley  JRTangel  DJMezzanotte  WSWhite  DP Influence of sleep on response to negative airway pressure of tensor palatini muscle and retropalatal airway. J Appl Physiol. 1993;752117- 2124
8.
Carlson  DMCarley  DWOnal  ELopata  MBasner  RC Acoustically induced cortical arousal increases phasic pharyngeal muscle and diaphragmatic EMG in NREM sleep. J Appl Physiol. 1994;761153- 1159
9.
Tangel  DJMezzanotte  WSWhite  DP Influences of NREM sleep on activity of palatoglossus and levator palatini muscles in normal men. J Appl Physiol. 1995;78689- 695
10.
Tangel  DJMezzanotte  WSWhite  DP Influence of sleep on tensor palatini EMG and upper airway resistance in normal men. J Appl Physiol. 1991;702574- 2581
11.
Mezzanotte  WSTangel  DJWhite  DP Influence of sleep onset on upper airway muscle activity in apnea patients versus normal controls. Am J Respir Crit Care Med. 1996;1531880- 1887Article
12.
Carlson  DMOnal  ECarley  DWLopata  MBasner  RC Palatal muscle electromyogram activity in obstructive sleep apnea. Am J Respir Crit Care Med. 1995;1521022- 1027Article
13.
Schwartz  ARThut  DCBrower  RG  et al.  Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2J Appl Physiol. 1993;741597- 1605Article
14.
Seelagy  MMSchwartz  ARRuss  DBKing  EDWise  RASmith  PL Reflex modulation of airflow dynamics through the upper airway. J Appl Physiol. 1994;762692- 2700
15.
Rowley  JAWilliams  BCSmith  PLSchwartz  AR Neuromuscular activity and upper airway collapsibility: mechanisms of action in the decerebrate cat. Am J Respir Crit Care Med. 1997;156515- 521Article
16.
Eisele  DWSchwartz  ARHari  AThut  DCSmith  PL The effect of selective nerve stimulation on upper airway airflow mechanics. Arch Otolaryngol Head Neck Surg. 1995;1211361- 1364Article
17.
Kirsten  EBSt. John  WM A feline decerebration technique with low mortality and longterm homeostasis J Pharmacol Methods. 1978;1263- 268Article
18.
Thut  DCSchwartz  ARRoach  DWise  RAPermutt  SSmith  PL Tracheal and neck position influence upper airway airflow dynamics by altering airway length. J Appl Physiol. 1993;752084- 2090
19.
Rowley  JAPermutt  SWilley  SJSmith  PLSchwartz  AR Effect of tracheal and tongue displacement on upper airway airflow dynamics. J Appl Physiol. 1996;802171- 2178
20.
Smith  PLWise  RAGold  ARSchwartz  ARPermutt  S Upper airway pressure flow relationships in obstructive sleep apnea. J Appl Physiol. 1989;64789- 795
21.
van Lunteren  EStrohl  KP The muscles of the upper airway. Clin Chest Med. 1986;7171- 188
22.
Roberts  JLReed  WRThach  BT Pharyngeal airway stabilizing function of sternohyoid and sternothyroid muscles in the rabbit. J Appl Physiol Respir Environ Exerc Physiol. 1984;571790- 1795
23.
Schwartz  ARThut  DCRuss  DB  et al.  Effect of electrical stimulation of the hypoglossal nerve on airflow mechanics in the isolated upper airway. Am Rev Respir Dis. 1993;1471144- 1150Article
24.
Brennick  MJParisi  RAEngland  SJ Influence of preload and afterload on genioglossus muscle length in awake goats. Am J Respir Crit Care Med. 1997;1552010- 2017Article
Original Article
September 1999

The Effect of Tensor Veli Palatini Stimulation on Upper Airway Patency

Author Affiliations

From the Department of Otolaryngology–Head and Neck Surgery (Drs McWhorter and Eisele), and Division of Pulmonary and Critical Care Medicine, Department of Medicine (Drs Rowley, Smith, and Schwartz), The Johns Hopkins University School of Medicine, Baltimore, Md. Dr Rowley is now with the Division of Pulmonary and Critical Care Medicine, Department of Medicine, Wayne State University School of Medicine, Detroit, Mich.

Arch Otolaryngol Head Neck Surg. 1999;125(9):937-940. doi:10.1001/archotol.125.9.937
Abstract

Objective  To evaluate the effect of selective electrical stimulation of the tensor veli palatini muscle on upper airway patency.

Methods  Pressure-flow relationships were evaluated, in a feline isolated upper airway preparation, to determine the role of the soft palate musculature on airflow dynamics. The tensor veli palatini muscles were selectively stimulated while monitoring upper airway collapsibility (critical pressure), maximal inspiratory airflow, and the nasal resistance upstream to the flow-limiting site.

Results  Tensor veli palatini stimulation resulted (mean±SEM) in an increase in maximal inspiratory airflow from 74±13 mL/s to 93±18 mL/s (P=.04). The increase in maximal inspiratory airflow was associated with a decrease in critical pressure from −2.3±1.7 cm H2O to −4.7±2.7 cm H2O (P=.01) and an increase in nasal resistance from 32.4±24.3 cm H2O·L−1·s−1 to 50.8±29.7 cm H2O·L−1·s−1(P=.02).

Conclusions  Tensor veli palatini stimulation decreases upper airway collapsibility and is likely an integral component in maintaining airway patency. However, the effects of the isolated tensor veli palatini muscles are less significant than those seen previously with physiologic stimuli such as hypercapnia. These findings suggest that upper airway patency, although contributed to by the tensor veli palatini, requires the coordinated activation of palatopharyngeal muscles to adequately influence upper airway collapsibility.

COLLAPSE of the upper airway in patients with obstructive sleep apnea has been shown to occur in the nasopharynx, oropharynx, or hypopharynx.1 In recent years, upper airway research has increasingly focused on the nasopharynx, which may be the primary site of collapse in the majority of patients with obstructive sleep apnea.1,2 Collapse at this site may be due to disturbances in the neuromuscular control of the palatal musculature.

The tensor veli palatini, levator veli palatini, palatoglossus, palatopharyngeus, and the uvulae muscles are the 5 muscles that compose the palatal musculature. In both animals and humans, hypoxia,3 hypercapnia,35 resistive loading,4 negative pressure,6,7 and acoustic stimuli8 augment the electromyographic activity of the tensor veli palatini and the levator veli palatini. Moreover, investigators have demonstrated that the tonic activity of these muscles decreases at sleep onset9,10 and the neuromuscular response of these muscles to negative pressure decreases during sleep.7 Thus, it has been postulated that a defect in the neuromuscular control of the palatal muscles predisposes to collapse and airflow obstruction in patients with obstructive sleep apnea.11,12

We have previously studied the relationships between neuromuscular activity and airflow dynamics through the upper airway using a feline isolated upper airway model.1316 In this preparation, when the pharyngeal airway pressure falls below the critical airway pressure (Pcrit), the upper airway airflow is limited. The maximal airflow at flow limitation (V̇Imax) is determined by Pcrit, which can be considered a measure of airway collapsibility, and by the resistance of the relatively rigid segment upstream from the flow limiting site (nasal resistance; Rn). A unique feature of this model is that the soft palate is the site of obstruction. However, the influence of the palatal musculature on the severity of airflow obstruction in this preparation has not been previously studied.

To better understand the role of the palatal musculature, we chose to study the effect of the tensor veli palatini muscle stimulation on upper airway airflow dynamics. The tensor veli palatini muscle was chosen for study over the levator veli palatini because of its mechanism of action and more prominent role during respiration. The tensor veli palatini originates in the scaphoid fossa and hooks over the pterygoid hamulus and inserts in the midline aponeurosis of the palate (Figure 1). The change in orientation over the hamulus tenses the palate in a lateral direction, whereas the levator veli palatini elevates the palate. Based on this action, we hypothesized that increased activity of the tensor veli palatini would decrease the collapsibility of the pharyngeal airway at the level of the soft palate. Therefore, the purpose of this investigation was to determine the effect of selective stimulation of the tensor veli palatini muscle on upper airway collapsibility in the isolated upper airway model.

METHODS

Institutional guidelines regarding animal experimentation were followed, and all experiments were approved by the Animal Use Committee of The Johns Hopkins University School of Medicine, Baltimore, Md. The study was performed in 5 supine male cats, weighing 2 to 2.5 kg, premedicated with an intramuscular injection of xylazine hydrochloride (3 mg/kg) and anesthetized with ketamine hydrochloride (50 mg/kg). Blood pressure was monitored through a femoral arterial line and maintained with isotonic sodium chloride solution given through a femoral vein. The cranium was exposed, and midcollicular decerebration was performed.17

A feline isolated upper airway preparation was used as previously described.14,18 To prepare the isolated upper airway, the cervical trachea was transected and the distal end was cannulated with an endotracheal tube (5 mm inner diameter), through which the animal breathed spontaneously. A rigid cannula (3 mm inner diameter, 2 cm in length) was inserted into the proximal trachea and secured at the level of the aryepiglottic folds. To monitor respiration, an esophageal balloon was inserted into the lower esophagus. During the collection of data, the tongue was allowed to prolapse into the mouth and the lips were sutured shut with a purse-string suture. The cat's head was fixed in place at an angle of approximately 50° to 60° from the horizontal plane. The epiglottis was left undisturbed in its normal anatomic position.

A surgical technique was devised to isolate the tensor palatini muscles using an approach through a midline cervical incision. Care was taken to avoid injury to the nerves, blood vessels, and mucosa. Dissection was carried out superiorly, anterolateral to the carotid sheath, to the level of the skull base where the pterygoid hamulus was identified by palpation. The tensor veli palatini muscle was identified as it turned over the hook of the hamulus and spread into an aponeurosis for insertion at the midline raphe. The vertical portion of the tensor veli palatini was isolated by blunt dissection circumferentially around the muscle, between the scaphoid fossa and pterygoid hamulus (Figure 1). Latex finger cots were placed under the tensor veli palatini muscles to isolate the muscles and to ensure selective electrical stimulation of the tensor veli palatini muscles.

To electrically stimulate the tensor veli palatini muscles, Teflon-coated fine-wire needle electrodes were placed into the bellies of the 2 tensor veli palatini muscles and connected to a constant current electrical stimulator (Transcutaneous Electrical Nerve Stimulator; Medtronic, Inc, Minneapolis, Minn). The tensor veli palatini muscles were stimulated at 50 Hz with a supramaximal voltage and a pulse duration of 40 microseconds. Selective stimulation of the tensor veli palatini muscles was confirmed by visual inspection. The muscle bellies were noted to visibly contract and a marked tensing of the soft palate was observed with stimulation.

A vacuum source was applied to the proximal trachea to generate inspiratory flow through the isolated upper airway. Pressure-flow recordings were made during the inspiratory phase of the respiratory cycle of the spontaneously breathing cats, as previously described, to determine the V̇Imax as well as Pcrit and Rn.1316,18,19 The tensor veli palatini muscles were then electrically stimulated just prior to an inspiratory effort, and the pressure-flow recordings were repeated during maximal stimulation. This series of measurements was repeated 5 to 6 times for each condition in each of the 5 decerebrated cats. The measurements were reproducible for each condition in each cat.

Data are presented as means ± SEMs for each measurement at each condition. A 1-way analysis of variance (Minitab Inc, State College, Penn) was used to compare the effects of stimulation with baseline. A significance level of P<.05 was used for all comparisons.

RESULTS

Figure 2 presents the results of the bilateral tensor veli palatini muscle stimulation for the 5 cats. The results are presented as V̇Imax (top panel), Pcrit (middle panel), and Rn (bottom panel) plotted before and after electrical stimulation. With stimulation of the bilateral tensor veli palatini muscles, V̇Imax, the maximal inspiratory inflow, increased from 74±13 mL/s to 93±18 mL/s (P=.04). The increase in V̇Imax was associated with a decrease in Pcrit from −2.3±1.7 cm H2O to −4.7±2.7 cm H2O (P=.01). The upstream nasal resistance, Rn, increased from 32.4±24.3 cm H2O·L−1·s−1 to 50.8±29.7 cm H2O·L−1·s−1 (P=.02).

COMMENT

In recent years, uvulopalatopharyngoplasty has become the most commonly performed surgical therapy for obstructive sleep apnea. Unfortunately, there remains a 50% failure rate for the surgery, with few selection criteria identified to predict a positive outcome. Consequently, a great deal of research has been focused on the palate, and particularly the tensor veli palatini muscle, to help understand its role in the pathogenesis of obstructive sleep apnea. In dog models, the tensor veli palatini has been shown to have inspiratory phasic activity that is augmented by hypercapnia, hypoxemia, and negative upper airway pressure.3,6 In humans, investigators have shown the tonic activity of the tensor veli palatini decreases with the onset of sleep,11 and the augmented tensor veli palatini activity seen with negative upper airway pressure is attenuated during sleep.7 Thus, it has been postulated that a loss of tensor veli palatini activity may lead to upper airway collapse in patients with obstructive sleep apnea.11,12 Nevertheless, the influences of changes in tensor veli palatini muscle activity on airflow dynamics are not well understood.

We have used a feline isolated upper airway model to examine the neuromuscular mechanisms modulating maximal airflow through the upper airway.1315 This model reproduces the condition of pharyngeal airflow obstruction and inspiratory flow limitation that characterizes human sleep-disordered breathing.20 The model has further allowed us to determine the effect of individual muscles on V̇Imax,15 and whether changes observed in V̇Imax were due to changes in pharyngeal collapsibility (Pcrit) or resistance (Rn) upstream to the site of obstruction. In the present study, we used this model to investigate the role played by the tensor veli palatini muscles in modulating the severity of upper airway airflow obstruction. Our results indicate that bilateral stimulation of the tensor veli palatini muscles leads to an increase in V̇Imax. The increase in V̇Imax is associated with a decrease in Pcrit, reflecting a decrease in palatal collapsibility at the site of airflow obstruction, and a concomitant increase in Rn. We conclude that tensor palatini stimulation increased V̇Imax by decreasing collapsibility, but the increase in V̇Imax was offset somewhat by a concomitant increase in the resistance upstream to the site of airway collapse.

One advantage of our experimental approach was that methods were developed to stimulate the tensor veli palatini muscles selectively. This allowed us to determine the influence of the tensor veli palatini muscles on pharyngeal airflow dynamics without altering the activity of the other upper airway muscles. The tensor veli palatini muscles neither elevate nor depress the soft palate. Rather, their mechanism of action tenses the palate in a lateral direction.21 Accordingly, we can attribute observed decreases in Pcrit to increased tension within the soft palate itself. This finding is consistent with previous observations suggesting that Pcrit is influenced by changes in tension in the pharyngeal wall.15,18,19,22 In fact, earlier studies suggest such an increase in pharyngeal wall tension is associated with an increase in Rn.15 Thus, the increase in Rn that we observed in this study suggests that significant dilatation of the upper airway does not occur with tensor veli palatini muscle stimulation. Therefore, we believe stimulation of the tensor palatini muscles decreases Pcrit by increasing airway wall tension rather than by dilating the airway.

Although we found that V̇Imax and Pcrit changed significantly with tensor veli palatini muscle stimulation, we believe these changes were modest compared with those responses observed with previous experiments in this model. For example, we have shown hypercapnia produces large changes in both V̇Imax and Pcrit, presumably because of its more generalized stimulation of upper airway neuromuscular activity.14,15 With the cat breathing a hypercapnic air mixture, a 4.5-cm H2O decrease in Pcrit15 was observed, whereas with tensor veli palatini muscle stimulation, the mean decrease in Pcrit was 2.4 cm H2O. Similarly, selective stimulation of the genioglossus muscle produced even larger decreases in Pcrit, with an average decrease of 12.0 cm H2O,16,23 suggesting that other muscles may play a greater role in the control of pharyngeal collapsibility. It appears, therefore, that activation of several muscles is responsible for the changes in Pcrit seen during hypercapnia. This is not surprising given the anatomic complexity of the upper airway. Moreover, we and others have previously demonstrated that length-tension relationships of specific upper airway muscles may play a role in modulating pharyngeal collapsibility.15,19,24 Therefore, we suggest that the coordinated activation of the palatopharyngeal muscles helps achieve an airway configuration that maximally increases upper airway tension and decreases pharyngeal collapsibility.

In summary, selective bilateral electrical stimulation of the tensor veli palatini muscles leads to a decrease in collapsibility in an isolated upper airway feline model. We speculate the decreased collapsibility is related to increased tension of the palate when the tensor veli palatini muscles are electrically stimulated. Selective stimulation of the tensor veli palatini muscles, however, results in airflow dynamics changes that are only modest by comparison to those produced by more generalized neuromuscular stimulation. This suggests that other upper airway muscles are also involved in the modulation of upper airway collapsibility. These data also suggest other sites in the airway may be the locus of airway collapse, and the effect of the palatal tensing may be less than that required for therapeutic effect in the treatment of obstructive sleep apnea. This work might be applied to uvulopalatopharyngoplasty failure. From this, one might infer that palatal stiffening does not completely alleviate flow obstruction. Additional work should be conducted to determine if stimulation of the tensor veli palatini muscles would be a predictor of good outcome following uvulopalatopharyngoplasty.

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Article Information

Accepted for publication March 11, 1999.

Corresponding author: David W. Eisele, MD, The Johns Hopkins Hospital, PO Box 41402, Baltimore, MD 21203-6402.

References
1.
Morrison  DLLaunois  SHIsono  SFeroah  TRWhitelaw  WARemmers  JE Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea. Am Rev Respir Dis. 1993;148606- 611Article
2.
Horner  RLShea  SAMcIvor  JGuz  A Pharyngeal size and shape during wakefulness and sleep in patients with obstructive sleep apnea. Q J Med. 1989;268719- 735
3.
Kogo  MKurimoto  TKoizumi  HNishio  JMatsuya  T Respiratory activities in relation to palatal muscle contraction. Cleft Palate Craniofac J. 1992;29174- 178Article
4.
Tangel  DJMezzanotte  WSWhite  DP Respiratory related control of palatoglossus and levator palatini muscle activity. J Appl Physiol. 1995;78680- 688
5.
Launois  SHRemsburg  SYang  WJWeiss  JW Relationship between velopharyngeal dimensions and palatal EMG during progressive hypercapnia. J Appl Physiol. 1996;80478- 485
6.
van der Touw  TO'Neill  NBrancatisano  AAmis  TWheatley  JREngel  LA Respiratory related activity of soft palate muscles: augmentation by negative upper airway pressure. J Appl Physiol. 1994;6424- 432
7.
Wheatley  JRTangel  DJMezzanotte  WSWhite  DP Influence of sleep on response to negative airway pressure of tensor palatini muscle and retropalatal airway. J Appl Physiol. 1993;752117- 2124
8.
Carlson  DMCarley  DWOnal  ELopata  MBasner  RC Acoustically induced cortical arousal increases phasic pharyngeal muscle and diaphragmatic EMG in NREM sleep. J Appl Physiol. 1994;761153- 1159
9.
Tangel  DJMezzanotte  WSWhite  DP Influences of NREM sleep on activity of palatoglossus and levator palatini muscles in normal men. J Appl Physiol. 1995;78689- 695
10.
Tangel  DJMezzanotte  WSWhite  DP Influence of sleep on tensor palatini EMG and upper airway resistance in normal men. J Appl Physiol. 1991;702574- 2581
11.
Mezzanotte  WSTangel  DJWhite  DP Influence of sleep onset on upper airway muscle activity in apnea patients versus normal controls. Am J Respir Crit Care Med. 1996;1531880- 1887Article
12.
Carlson  DMOnal  ECarley  DWLopata  MBasner  RC Palatal muscle electromyogram activity in obstructive sleep apnea. Am J Respir Crit Care Med. 1995;1521022- 1027Article
13.
Schwartz  ARThut  DCBrower  RG  et al.  Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2J Appl Physiol. 1993;741597- 1605Article
14.
Seelagy  MMSchwartz  ARRuss  DBKing  EDWise  RASmith  PL Reflex modulation of airflow dynamics through the upper airway. J Appl Physiol. 1994;762692- 2700
15.
Rowley  JAWilliams  BCSmith  PLSchwartz  AR Neuromuscular activity and upper airway collapsibility: mechanisms of action in the decerebrate cat. Am J Respir Crit Care Med. 1997;156515- 521Article
16.
Eisele  DWSchwartz  ARHari  AThut  DCSmith  PL The effect of selective nerve stimulation on upper airway airflow mechanics. Arch Otolaryngol Head Neck Surg. 1995;1211361- 1364Article
17.
Kirsten  EBSt. John  WM A feline decerebration technique with low mortality and longterm homeostasis J Pharmacol Methods. 1978;1263- 268Article
18.
Thut  DCSchwartz  ARRoach  DWise  RAPermutt  SSmith  PL Tracheal and neck position influence upper airway airflow dynamics by altering airway length. J Appl Physiol. 1993;752084- 2090
19.
Rowley  JAPermutt  SWilley  SJSmith  PLSchwartz  AR Effect of tracheal and tongue displacement on upper airway airflow dynamics. J Appl Physiol. 1996;802171- 2178
20.
Smith  PLWise  RAGold  ARSchwartz  ARPermutt  S Upper airway pressure flow relationships in obstructive sleep apnea. J Appl Physiol. 1989;64789- 795
21.
van Lunteren  EStrohl  KP The muscles of the upper airway. Clin Chest Med. 1986;7171- 188
22.
Roberts  JLReed  WRThach  BT Pharyngeal airway stabilizing function of sternohyoid and sternothyroid muscles in the rabbit. J Appl Physiol Respir Environ Exerc Physiol. 1984;571790- 1795
23.
Schwartz  ARThut  DCRuss  DB  et al.  Effect of electrical stimulation of the hypoglossal nerve on airflow mechanics in the isolated upper airway. Am Rev Respir Dis. 1993;1471144- 1150Article
24.
Brennick  MJParisi  RAEngland  SJ Influence of preload and afterload on genioglossus muscle length in awake goats. Am J Respir Crit Care Med. 1997;1552010- 2017Article
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