Download Soft palate muscle responses to negative upper airway pressure

Soft palate muscle responses
to negative upper airway pressure
T. C. AMIS, N. O’NEILL, J. R. WHEATLEY, T. VAN DER TOUW,
E. DI SOMMA, AND A. BRANCATISANO
Department of Respiratory Medicine, Westmead Hospital,
and University of Sydney, Westmead, New South Wales 2145, Australia
soft palate muscles; negative pressure; superior laryngeal
nerve
RETROPALATAL AIRWAY PATENCY is controlled via soft
palate muscle activity (20), and, during sleep, this
segment of the upper airway is a major site of narrowing in both normal humans (6) and patients with the
obstructive sleep apnea (OSA) syndrome (5). Consequently, depression of soft palate muscle activity during sleep, with resultant impaired defense of retropalatal airway caliber, has emerged as a potentially
important factor in the pathogenesis of OSA (21, 25).
Negative pressure within the upper airway lumen
(NUAP) is a well-recognized and potent stimulus for
the reflex recruitment of upper airway dilator muscle
activity. Upper airway muscles known to be responsive
to NUAP include the alae nasi (23), genioglossus (3, 4,
14, 23, 24), cricothyroid (13), posterior cricoarytenoid
(13, 23), and sternohyoid and sternothyroid (13). The
tensor veli palatini (25), levator veli palatini (18),
palatoglossus (18, 19), and palatopharyngeus (17)
muscles are also reported to be recruited by NUAP.
Negative pressure recruitment of upper airway
electromyographic muscle (EMG) activity is mediated
via a reflex response originating from upper airway
mechanoreceptors (8, 9, 15, 27) and having afferent
pathways thought to involve the trigeminal, glossopharyngeal, and superior laryngeal nerves. Thus, for
muscles such as the genioglossus, receptors located in
the nasal, pharyngeal, and laryngeal segments of the
upper airway are reportedly involved (2, 8, 9, 15) in the
response. The implication from such a distribution of
receptor sites is that exposure of any single upper
airway segment to NUAP will result in the global
recruitment of upper airway dilator muscle activity.
However, the soft palate contains both elevator and
depressor muscles. Consequently, the resultant effect
(on upper airway geometry) of global recruitment of
palatal muscles is likely to depend on interactions
between anatagonists, which, in turn, will depend on
relative mechanical advantage and the responsiveness
of individual muscles to NUAP.
The afferent pathways for augmentation of soft palate muscle activity with NUAP have not been defined
(25). Consequently, the relative contribution (to soft
palate muscle recruitment) of receptors located in
different topographical zones of the upper airway is not
understood. Furthermore, in a previous study in dogs
(22), recruitment of individual soft palate muscles by
NUAP varied, with recruitment of levator being the
least reproducible of the muscles studied. This finding
has led us to hypothesize that there are differences in
the linkage of individual soft palate muscles to the
NUAP reflex (i.e., muscle-specific reflex responses). In
addition, the magnitude of individual soft palate muscle
responses to differing levels of NUAP (i.e., stimulusresponse characteristics) have not been defined. The
strength of the response of individual soft palate muscles
to NUAP is relevant to their ability to contribute to the
resolution and prevention of obstructive apneas in
OSA.
Thus the aims of the present study were as follows: 1)
localize the negative-pressure-sensitive zones within
the upper airway that participate in the NUAPmediated reflex recruitment of individual palatal
muscles and 2) define stimulus-response characteristics for recruitment of individual palatal muscles with
NUAP.
METHODS
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http://www.jap.org
We studied 11 adult crossbred dogs (5 males, 6 females)
under general anaesthesia induced by intravenous pentobarbital sodium (25–30 mg/kg) followed by intravenous a-chloralose (initial dose 25 mg/kg). Anesthesia was maintained with
8750-7587/99 $5.00 Copyright r 1999 the American Physiological Society
523
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Amis, T. C., N. O’Neill, J. R. Wheatley, T. Van der Touw,
E. Di Somma, and A. Brancatisano. Soft palate muscle
responses to negative upper airway pressure. J. Appl. Physiol.
86(2): 523–530, 1999.—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 210 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.
524
PALATAL MUSCLE RESPONSES TO UPPER AIRWAY PRESSURE
an intermittent infusion of a 0.5% a-chloralose solution
administered via a cannula inserted into a femoral vein.
a-Chloralose produces stable, long-lasting, light anesthesia
and has been used widely in animal studies examining upper
airway reflexes (11, 23, 26). Anesthesia levels were adjusted,
as necessary, to maintain a stable heart rate and blood
pressure throughout the study. Seven of the animals were
also part of a previous study in which responses of the
genioglossus and hyoepiglotticus muscles to NUAP were
examined (1). The investigation was approved by the Western
Sydney Area Health Service Animal Care and Ethics Committee.
Experimental Preparation
Bipolar Teflon-coated fine-wire electrodes (40 gauge) were
inserted per orally via a 23-gauge hypodermic needle into
each soft palate muscle by using a technique we have
described previously (22). Electrodes were placed unilaterally
in the tensor, levator, and palatinus muscles (equivalent to
the human musculus uvulae). Placement of the electrodes in
each muscle was confirmed by visual observation of soft
palate movements during tetanic low-voltage electrical stimulation (model S48 Grass stimulator, 5–7 V, 2-s duration, 40
pulses/s, 0.2 ms/pulse) applied via the fine-wire electrodes.
Correct placement of the electrodes was accepted only when
specific soft palate movements characteristic for each soft
palate muscle (22) and unaccompanied by visual movement of
any other structures were observed during electrical stimulation.
The raw EMG signal was filtered (80–1,000 Hz), amplified,
rectified, and integrated (model NT1900, Neotrace) with a
time constant of 100 ms to produce a moving time average
(MTA) EMG. In addition, the raw EMG was displayed on an
oscilloscope as well as transformed into an audio signal via an
amplifier and loudspeaker. These visual and auditory signals
were used to determine the presence of action potentials in
the raw EMG signal.
Data Recording
The volume, pressure, and integrated EMG signals were
recorded on a strip-chart recorder (model 7758B, HewlettPackard).
Experimental Protocol
Measurements of soft palate muscle MTA EMG activity
were obtained during quiet tidal tracheostomy breathing
(control) and during progressive sequential (0 to 240 cmH2O
in 25-cmH2O steps) or single-step (0 to 210, 0 to 220, and 0
to 232 to 240 cmH2O) changes in NUAP. The NUAP was
applied to either the nasal (via the face mask) or laryngeal
end of the isolated upper airway, via the cranial tracheal
cannula in group 1 dogs or via the retrograded endotracheal
tube in group 2 dogs. Each NUAP stimulus was applied for
5–10 breaths. One to two runs of progressive sequential
NUAP were obtained for each condition in each dog, whereas
one to three runs were obtained for the single-step changes in
NUAP. In seven dogs, studies were performed before and
after bilateral section of the SLNin.
Data Analysis
The MTA EMG activity was quantified in arbitrary units
(AU) above baseline (i.e., where the raw EMG did not show
any action potentials). Timing of the soft palate muscle MTA
EMG signal was related to the VT signal. Peak inspiratory
and peak expiratory MTA EMG activity was measured as the
maximum value of MTA EMG activity during inspiration and
expiration, respectively. Tonic activity was defined as the
minimum value of MTA EMG measured above baseline. The
EMG activity was measured for four to six representative
breaths, usually the five breaths immediately preceding
NUAP for control and the first five breaths after application of
NUAP. These data were averaged to produce single control
and intervention values for each NUAP challenge. The data
from repeated runs were then averaged and expressed as
single values at each NUAP level for each dog.
The analysis of the topographical distribution of responses
to NUAP was confined to an analysis of changes in EMG
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The animals were studied supine with the mouth closed
and secured with tape. A tight-fitting face mask was sealed to
the animal’s muzzle. Pressure in the mask was measured
with a pressure transducer (6100 cmH2O, Celesco Transducer Products, IDM Instruments, Dandenong, Victoria, Australia).
The trachea was divided between the fourth and fifth
cartilage rings caudal to the cricoid cartilage. Care was taken
to preserve the recurrent laryngeal nerves. Separate tracheal
cannulas were inserted and fastened to the cranial and
caudal cut ends of the trachea. Airflow was measured at
the caudal tracheal cannula with a pneumotachograph
(Fleisch no. 1) coupled to a differential pressure transducer
(MP 45, 65 cmH2O, Validyne, Northridge, CA). Tidal volume
(VT ) was measured by electrical integration of the flow signal.
In six dogs (group 1), pressure in the laryngeal lumen was
measured with a pressure transducer attached to a side port
on the cranial tracheal cannula. With the use of three-way
taps, a high-impedance negative-pressure source was connected to either the cranial tracheal cannula or the face mask,
thus allowing a constant negative pressure to be applied to
the nasal or laryngeal end of the isolated and sealed upper
airway.
The remaining five animals (group 2) were prepared in an
identical manner except that a cuffed endotracheal tube
(internal diameter 5.0 mm, external diameter 6.9 mm, length
23 cm, Mallinckrodt) was passed into the nasopharyngeal
airway via the cranial tracheal cannula. The tip of this tube
was placed at the nasal choanae, and the cuff was inflated.
Negative pressure was then applied to the airway via the
endotracheal tube with the applied pressure measured at
the caudal end of the tube via a pressure transducer (MP 45,
6100 cmH2O, Validyne). The cuff was then deflated, and the
tip of the tube was moved caudally by 2–4 cm. The cuff was
then inflated, and negative pressure was reapplied. This
procedure was repeated until the tip of the tube was caudal to
the glottis and in the cranial trachea. In this manner,
systematically longer segments of the nasopharyngeal airway were exposed to the NUAP stimulus. The position of the
tip of the tube was assessed from a distance scale marked on
the tube at the commencement of the study when, with the
mouth open, the position of the tube could be related visually
and by palpation to upper airway structures (i.e., glottis, tip
of epiglottis, and nasal choanae). In all group 2 dogs, the
cranial tracheal cannula (and laryngeal lumen) was open to
the atmosphere for all measurements except those in which
the endotracheal tube tip was caudal to the glottis.
In seven of the dogs, the internal branches of the superior
laryngeal nerve (SLNin) were identified bilaterally at their
entrance to the thyrohyoid membrane and then were separated from surrounding structures and tagged for later
identification and section.
EMG
PALATAL MUSCLE RESPONSES TO UPPER AIRWAY PRESSURE
RESULTS
Transmision of NUAP Through the Upper Airway
In all group 1 dogs, the changes in NUAP applied at
either the larynx/cranial trachea or the face mask were
not transmitted to the opposite end of the upper airway
for any NUAP level studied (Fig. 1). In the group 2 dogs,
NUAP was transmitted to the face mask in all cases
where the tip of the endotracheal tube was at the nasal
choanae. Transmission also occurred to varying degrees as the tube was moved caudally. When the tube
was in the cranial trachea, partial transmission of the
pressure stimulus (,5–50%) to the face mask occurred
in three dogs.
Laryngeal NUAP Application: SLNin Intact
Palatinus. Data for palatinus MTA EMG activity
were obtained in 10 dogs. During control conditions,
respiratory-related phasic inspiratory palatinus MTA
EMG activity was detected in six dogs, phasic expira-
Fig. 1. Strip-chart recording for 1 dog from group 1 showing the following from top to bottom: moving time average
(MTA) EMG activity in arbitrary units of the palatinus (PAL), levator veli palatini (LP), and tensor veli palatini
(TP); tidal volume (VT ), and pressure in the face mask (Pmask) and laryngeal lumen (Plarynx). Shown is single-step
application of 210 cmH2O pressure to 1) laryngeal/cranial tracheal end [Laryngeal negative upper airway pressure
(NUAP)], 2) nasal end (Nasal NUAP) of isolated upper airway [with internal branches of superior laryngeal nerves
(SLNin) intact], and 3) laryngeal/cranial tracheal end of upper airway after bilateral section of SLNin (Laryngeal
NUAP-SLNin Cut). Insp, inspiration; 0, baseline EMG activity. Amplifier gains shown as 32 and 35 (lower
numbers represent higher amplification). Note gain change for LP and TP in panel at right. Arrows on EMG traces
indicate onset of NUAP.
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activity with NUAP of between 220 and 240 cmH2O. Distance along the upper airway was expressed as a percentage
of the total distance from the nasal choanae (0%) to the glottis
(100%). Group mean data were then analyzed for three zones
in the nasopharyngeal airway: 1) measurements obtained at
all sites ,70% of the distance from the nasal choanae to the
glottis, i.e., rostral zone; 2) measurements obtained between
the 70% distance point and the glottis, i.e., epiglottic zone;
and 3) measurements obtained with NUAP applied below the
glottis, i.e., subglottic zone.
Group 1 and group 2 dogs showed similar responses; hence
the data, where applicable, have been pooled for analysis.
Similar findings were also obtained for both single-step and
progressive graded changes for the same level of NUAP (P .
0.05); consequently, these data have also been pooled for
analysis. Statistical comparisons were made by using a
paired t-test for single-condition paired data and ANOVA
(with appropriate adjustment where neccessary for unbalanced data) for multiple-condition comparisons. Fisher’s protected least significant difference test was used as a post hoc
multiple-comparison technique. P , 0.05 was taken as significant.
525
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PALATAL MUSCLE RESPONSES TO UPPER AIRWAY PRESSURE
tory activity was found in four dogs, and low-level tonic
activity was present in three dogs. Application of
laryngeal NUAP increased palatinus peak inspiratory
EMG (by .0.5 AU) in 94% of 128 trials, peak expiratory
EMG in 66%, and tonic EMG in 64%. Figure 1 shows
the response to a single-step change in NUAP of 0 to
210 cmH2O in one dog.
Compared with control values, peak inspiratory palatinus EMG activity increased significantly with all
levels of NUAP (P , 0.05; Fig. 2A). Peak expiratory
activity also increased significantly with all levels of
NUAP less than 25 cmH2O (P , 0.05; Fig. 2B),
whereas tonic activity increased with all levels of
NUAP less than 210 cmH2O (P , 0.05; Fig. 2C).
Beyond 210 cmH2O, larger decreases in NUAP (up to
240 cmH2O) did not result in any significant (P . 0.05)
further augmentation of palatinus EMG activity (Fig. 2).
Tensor veli palatini. Data for tensor MTA EMG
activity were obtained in 10 dogs. During control
Fig. 2. Group mean data for peak inspiratory (PI; A), peak expiratory
(PE; B), and tonic (T; C) MTA EMG of palatinus muscle vs. pressure
at larynx or nares (Pressure). Data are shown for application of
progressive sequential negative pressure steps (NUAP) at larynx/
cranial trachea (r; n 5 10 dogs) and nares (j; n 5 9 dogs), both with
SLNin intact, and at larynx/cranial trachea after bilateral section of
SLNin (s; n 5 6 dogs). au, Arbitrary units. Bars, 61 SE. * P , 0.05,
compared with value at 0 cmH2O.
conditions, respiratory-related phasic inspiratory tensor EMG activity was detected in six dogs, phasic
expiratory activity was found in six dogs, and low-level
tonic activity was present in six dogs. Application of
laryngeal NUAP increased peak inspiratory tensor
MTA EMG in 74% of 132 trials, peak expiratory EMG in
30%, and tonic EMG in 32%.
Compared with control values, peak inspiratory (but
not peak expiratory or tonic) tensor veli palatini EMG
activity increased significantly with all levels of NUAP
less than 25 cmH2O (P , 0.05; Fig. 3). Beyond 210
cmH2O, larger decreases in NUAP (up to 240 cmH2O)
did not result in any significant (P . 0.05) further
augmentation of tensor EMG activity (Fig. 3).
Levator veli palatini. Data for levator MTA EMG
activity were obtained from nine dogs. During control
conditions, respiratory-related phasic inspiratory levator EMG activity was detected in four dogs and phasic
expiratory activity in five animals. No tonic activity
was present in any dog. Application of laryngeal NUAP
resulted in variable EMG responses. Peak inspiratory
levator EMG increased in only 43% of 118 trials. Peak
expiratory and tonic activity increased in only 9 and
10% of trials, respectively. Consequently, there was no
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Fig. 3. Group mean data for PI (A), PE (B), and T (C) MTA EMG of
tensor veli palatini muscle vs. pressure at larynx or nares (Pressure).
Data are shown for application of progressive sequential negative
pressure steps (NUAP) at larynx/cranial trachea (r; n 5 10 dogs) and
nares (j; n 5 10 dogs), both with SLNin intact, and at larynx/cranial
trachea after bilateral section of SLNin (s; n 5 6 dogs). Bars, 61 SE.
* P , 0.05 compared with value at 0 cmH2O.
PALATAL MUSCLE RESPONSES TO UPPER AIRWAY PRESSURE
527
peak inspiratory, peak expiratory, and tonic EMG activity failed to increase with the application of laryngeal
NUAP in the majority (.83%) of the 55 trials performed. There was no significant change in EMG
activity with any individual level of laryngeal NUAP
for any muscle (P . 0.05; Figs. 1–4).
Topographical Distribution of NUAP Responses
Fig. 4. Group mean data for PI (A), PE (B), and T (C) MTA EMG of
the levator veli palatini muscle vs. pressure at larynx or nares
(Pressure). Data are shown for application of progressive sequential
negative pressure steps (NUAP) at larynx/cranial trachea (r; n 5 9
dogs) and nares (j; n 5 10 dogs), both with SLNin intact, and at
larynx/cranial trachea after bilateral section of the SLNin (s; n 5 6
dogs). Bars, 61 SE. * P , 0.05 compared with value at 0 cmH2O.
significant (P .0.05) increase in levator veli palatini
EMG activity with any level of NUAP applied at the
larynx (Fig. 4).
Nasal NUAP Application: SLNin Intact
Data for MTA EMG activity during NUAP applied to
the nose (and not transmitted to the larynx) were
obtained in 9 dogs for palatinus and in 10 dogs for both
levator and tensor. In all three muscles, peak inspiratory, peak expiratory, and tonic EMG activity failed to
increase or decreased with the application of nasal
NUAP in the vast majority (.75%) of the 100–111
trials performed. There was no significant change in
EMG with any individual level of nasal NUAP for any
muscle (Figs. 1–4) except for a small, but significant
(P , 0.05), increase in tonic EMG activity for the
levator at a NUAP of 240 cmH2O (Fig. 4C). This mean
change was very small (0.1 AU) and, in fact, was beyond
the resolution of our measurement technique (0.5 AU).
Laryngeal NUAP Application: SLNin Cut
After section of the SLNin, data was obtained in six
dogs for each soft palate muscle. In all three muscles,
Fig. 5. A: change in PI palatinus muscle MTA EMG activity from
control and recorded during 189 applications of 220 to 240 cmH2O
NUAP to all sites in upper airway in 5 dogs. Distance along upper
airway has been expressed as percentage of total distance from nasal
choanae (NC) to glottis (G). Also shown is range of distances
encountered for epiglottic tip (ET). Note that there is considerable
overlap of data points such that total number of points visible on plot
is ,189. B: group mean (1SE) data (n 5 5 dogs) for change in PI, PE,
and T MTA EMG activity occurring with NUAP challenges applied at
rostral, epiglottic, and subglottic zones of upper airway. Dashed lines,
upper airway zones; dotted line, zero EMG change with NUAP. * P ,
0.05 compared with control. 1 P , 0.05 compared with rostral zone.
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Palatinus. When NUAP challenges (n 5 189) were
applied at different topographical sites within the
upper airway, there was no significant change in palatinus EMG activity within both the rostral (P . 0.5) and
epiglottic zones (P . 0.1). Within the subglottic zone,
peak inspiratory palatinus EMG increased significantly with NUAP (P 5 0.05; Fig. 5, A and B). Peak
expiratory and tonic activity also showed increases
with NUAP; however, these changes achieved only
borderline significance (P 5 0.06 and P 5 0.07, respectively; Fig. 5B). When the change in EMG activity with
NUAP was compared between zones, the changes in
peak inspiratory and peak expiratory EMG activity in
528
PALATAL MUSCLE RESPONSES TO UPPER AIRWAY PRESSURE
Fig. 7. A: change in PI levator veli palatini muscle MTA EMG
activity recorded during 183 applications of 220 to 240 cmH2O
NUAP to all sites in upper airway in 5 dogs. Distance along upper
airway has been expressed as percentage of total distance from NC to
G. Also shown is range of distances encountered for ET. Note that
there is considerable overlap of data points such that total number of
points visible on plot is ,183. B: group mean (1SE) data (n 5 5 dogs)
for change in PI, PE, and T MTA EMG activity occurring with NUAP
challenges applied at rostral, epiglottic, and subglottic zones of upper
airway. Dashed lines, upper airway zones; dotted line, zero EMG
change with NUAP. 1 P , 0.05 compared with rostral and epiglottic
zones.
in peak inspiratory EMG activity (but not peak expiratory or tonic activity) was significantly greater in the
subglottic zone than in the other two zones (P , 0.05,
Fig. 7).
DISCUSSION
Fig. 6. A: change in PI tensor veli palatini muscle MTA EMG activity
recorded during 197 applications of 220 to 240 cmH2O NUAP to all
sites in upper airway in 5 dogs. Distance along upper airway has been
expressed as percentage of total distance from NC to G. Also shown is
range of distances encountered for ET. Note that there is considerable
overlap of data points such that total number of points visible on plot
is ,197. B: group mean (1SE) data (n 5 5 dogs) for change in PI, PE,
and T MTA EMG activity occurring with NUAP challenges applied at
rostral, epiglottic, and subglottic zones of upper airway. Dashed lines,
upper airway zones; dotted line, zero EMG change with NUAP. * P ,
0.05 compared with control.
The principal findings in this study are that in
anesthetized, supine, tracheostomized, mouth-closed
dogs 1) tensor veli palatini and palatinus muscle EMG
activity is augmented by negative pressure in the
hypopharynx, larynx, and cranial trachea, 2) levator
veli palatini muscle EMG activity is weakly and inconsistently recruited by laryngeal NUAP, 3) NUAP applied exclusively to the nasal passages or nasopharynx
does not recruit soft palate muscle EMG activity, 4)
recruitment of soft palate muscle activity with NUAP is
mediated via the SLNin, and 5) the reflex activation of
soft palate muscles with NUAP is maximal with a
NUAP level of 210 cmH2O. In addition, it was observed
that in most dogs the upper airway remained closed
during the application of NUAP despite maximal
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the subglottic zone were significantly greater than
those in the rostral zone (P , 0.05). However, changes
in the epiglottic zone were not significantly different
from those in the other two zones (P . 0.05).
Tensor veli palatini. When NUAP challenges (n 5
197) were applied at different topographical sites within
the upper airway, changes in peak inspiratory, peak
expiratory, and tonic EMG activity of the tensor veli
palatini muscle were not significant within the rostral
(P . 0.4) and epiglottic (P . 0.1) zones. Within the
subglottic zone, peak expiratory and tonic EMG activity also did not change (P . 0.1). However, there was a
significant increase in peak inspiratory activity (P 5
0.04; Fig. 6, A and B). Although the changes in EMG
activity with NUAP tended to be greater in the epiglottic and subglottic zones (Fig. 6B), a significant difference (P . 0.1) between the zones was not detected.
Levator veli palatini. When NUAP challenges (n 5
183) were applied at different topographical sites within
the upper airway, there was no significant change in
levator veli palatini EMG activity within any zone (P .
0.08; Fig. 7, A and B). However, when the change in
EMG activity was compared between zones, the change
PALATAL MUSCLE RESPONSES TO UPPER AIRWAY PRESSURE
application of NUAP to the nasal cavity has been shown
to augment alae nasi and posterior cricoarytenoid
muscle activity in some studies (23, 26), whereas other
studies have attributed the response to NUAP almost
entirely to laryngeal afferents (11, 16). Furthermore,
Kaminuma and co-workers (11) reached the conclusion
that nasal pressure receptors have only minimal impact on the reflex recruitment of posterior cricoarytenoid muscle activity in dogs. The present study now
extends this conclusion to the canine soft palate muscles.
Some previous studies have suggested that the oropharynx is also not an important site for NUAP-related
reflex recruitment of genioglossus muscle activity (2).
Moreover, sectioning of the glossopharyngeal nerves in
cats increases rather than decreases the augmentation
of hypoglossal nerve activity with NUAP (8). Results
from the present study suggest that the pharynx is also
not important in the NUAP-mediated reflex recruitment of the soft palate muscles.
In the present study, laryngeal afferent activity appeared to be the only pathway for augmentation of soft
palate muscle activity by NUAP. We base this conclusion on the following results: 1) the response was not
elicited by nasal NUAP, 2) the response disappeared
after sectioning of the SLNin, and 3) the response was
confined to the epiglottic/laryngeal region of the upper
airway in the group 2 dogs. However, evidence obtained
in laryngectomized humans, in whom afferent impulses
from the larynx have been ablated, suggests that
genioglossus muscle EMG activity is still augmented by
NUAP (10), an effect attributed to receptors located in
the oropharyngeal and/or nasopharyngeal mucosa. This
evidence suggests that, at least in humans, pharyngeal
receptors do exist and may play an enhanced role in the
absence of laryngeal receptor input. However, in the
intact upper airway it seems that it is the laryngeal
receptors which play the dominant role.
The stimulus response characteristics for soft palate
muscle activation by graded NUAP have not been
previously studied over the range of NUAP employed in
the present study. The finding that there was no further
augmentation of soft palate muscle EMG activity by
NUAP beyond 210 cmH2O is similar to previously
reported data for other upper airway muscles (4, 17,
23). The plateau of reflex recruitment might be interpreted as representing maximal muscle EMG activation. However, we have previously observed spontaneous levels of soft palate muscle EMG activity during
upper airway breathing in anesthetized dogs (22) that
were two to four times higher than those measured at
an equivalent level of NUAP (211.3 6 1.8 cmH2O) to
that associated with the maximum EMG recruitment
in the present study. Plateauing of upper airway muscle
responses to NUAP may then suggest saturation of
receptor activation, with muscle EMG recruitment via
this reflex pathway limited to submaximal levels. Indeed, discharge frequencies of receptors generating
changes in afferent activity in the SLNin in response to
NUAP have been shown to reach plateau levels in the
27- to 228-cmH2O range in cats (9).
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NUAP-mediated reflex recruitment of soft palate muscle
activity.
Application of NUAP to the laryngeal end of the
upper airway (and not transmitted to the nose) consistently resulted in the recruitment of palatinus and
tensor veli palatini muscle EMG activity (see Figs.
1–3). This augmentation of EMG activity occurred on
the first breath after the change in NUAP (see Fig. 1).
Incomplete adaptation was observed with maintenance
of the stimulus being associated with a fall in response
compared with the first breath after application of
NUAP (see Fig. 1). This phenomenon has been reported
previously for other upper airway muscles (13) and also
in terms of the discharge of receptors (9).
The responses of the palatinus and tensor veli palatini muscles to laryngeal NUAP in the present study
are in general agreement with our previous findings in
dogs in which only a single level of NUAP was used (22)
and with those of Wheatley et al. (25) in humans.
However, the lack of consistent recruitment of the
levator veli palatini by laryngeal NUAP was surprising
in view of previous results demonstrating responses of
the levator to NUAP in humans (19) and animals (22).
The reason for this discrepancy is not entirely clear.
However, even in our previous study, some individual
animals did not show a levator response to NUAP (22).
In the present study, levator responses to NUAP were
small and variable. Because general anesthesia is
known to depress the recruitment of upper airway
muscles (7), the effect of anesthesia on levator activity
is a concern; however, a-chloralose produces light,
stable anesthesia, and all soft palate muscles within
each animal were studied concurrently. Consequently,
for the depressant effects of anesthesia to have been
responsible for the lack of recruitment of levator, this
would have had to have been a selective effect for this
muscle compared with the other soft palate muscles.
Thus the levator veli palatini in the dog appears to be
only inconsistently and weakly recruited in response to
NUAP applied at the larynx. This may also be the case
in humans because levator veli palatini EMG activity
in humans has been shown to have high inter- and
intrasubject variability both in terms of its activity
during quiet breathing and in its response to chemostimulation (12).
The complete loss of the response to laryngeal NUAP
after bilateral section of the SLNin is consistent with
results reported for the response of other upper airway
muscles to laryngeal NUAP (13, 15, 23) and establishes
that the SLNin is also the afferent pathway for soft
palate muscle recruitment.
When the NUAP was applied exclusively to the nasal
passages (and not transmitted to the larynx), there was
no augmentation of soft palate muscle EMG activity.
This finding suggests that local negative pressure
reflex control of soft palate muscle activity does not
involve receptors located in the nose. This conclusion
for the soft palate muscles is in contrast to results
reported for the genioglossus in rabbits, where nasal
NUAP (not transmitted to the larynx) has been shown
to recruit genioglossus EMG activity (15). In dogs, the
529
530
PALATAL MUSCLE RESPONSES TO UPPER AIRWAY PRESSURE
In conclusion, we have demonstrated that, in supine,
anesthetized dogs, reflex recruitment of soft palate
muscle activity by NUAP is predominantly modulated
by afferent activity originating from the laryngeal
and/or hypopharyngeal airway and transmitted via the
SLNin. The soft palate muscles may exhibit selective
recruitment in response to NUAP in that the levator
frequently failed to respond to NUAP, whereas the
palatinus and, to a lesser extent, tensor both consistently increased their activity. The response of the soft
palate muscles to NUAP reached a maximum at a
NUAP of 210 cmH2O; however, this level of activity
was insufficient to ensure a patent upper airway in
most dogs. Consequently, we speculate that NUAPmediated reflex recruitment of upper airway muscles,
including the soft palate muscles, may be more important in the prevention of upper airway collapse than in
the resolution of any resultant airway closure.
Received 16 March 1998; accepted in final form 14 October 1998.
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