UPPER AIRWAY PATENCY
Tracheal Traction Effects on Upper Airway Patency in Rabbits: The Role of Tissue
Pressure
Kristina Kairaitis, PhD1,2,3; Karen Byth, PhD2; Radha Parikh, PhD1,2; Rosie Stavrinou, BSc1,2; John R. Wheatley, PhD1,2,3; Terence C. Amis, PhD1,2,3
Ludwig Engel Centre for Respiratory Research; 2Westmead Millenium Research Institute; 3University of Sydney, Westmead Hospital, Westmead,
NSW, Australia.
1
decreased closing and reopening pressures by 1.4±0.2 cm H2O for 48g
of traction (n=13, P<0.0001). In addition, 48g of traction decreased ETPlat (at closure and reopening) by 0.2±0.05 cm H2O (P<0.0001), and decreased ETPant by 0.5±0.1 cm H2O at closing pressure and 0.8±0.1 cm
H2O at reopening (both p<0.0001). Thus, for 48 g of traction, PTMlat (at
closure and reopening) fell by 1.1±0.2 cm H2O and PTMant (reopening
only) fell by 0.9±0.3 cm H2O (all P<0.0001).
Conclusions: Since tracheal traction decreased PTMlat and PTMant by
a greater amount than ETPlat and ETPant, we conclude that the decrease
in upper airway collapsibility mediated by lung volume related caudal tracheal traction is partially explained by reductions in ETP.
Keywords: Upper airway extraluminal tissue pressure, tracheal traction,
upper airway patency
Citation: Kairaitis K; Byth K; Parikh R et al. Tracheal traction effects
on upper airway patency in rabbits: the role of tissue pressure. SLEEP
2006;30(2):179-186.
Study Objectives: To investigate the mechanisms via which lung volume
related caudal tracheal traction decreases upper airway collapsibility.
Design: Acute physiological study
Participants: 20 male, supine, anesthetised, tracheostomised, spontaneously breathing, NZ white rabbits fitted with a sealed face mask.
Setting: N/A
Measurements and Results: Upper airway extraluminal tissue pressure
(ETP) was measured in the lateral (ETPlat) and anterior (ETPant) pharyngeal walls (pressure transducer tipped catheters). Graded traction was applied to the isolated upper airway (n=17, 0-140g). Subsequently, inflation
and deflation was performed (with and without traction, 48g, n=13) with
measurement of intraluminal pressure. Upper airway transmural pressure
(PTM) was calculated (at closure and reopening) for both ETP sites (PTMlat and PTMant, respectively). A traction force of 144g decreased ETPlat
from 2.6±0.7 cm H2O (mean±SEM) to 2.1±0.7 cm H2O and ETPant from
1.1±0.4 cm H2O to 0.8±0.4 cm H2O (both P<0.001). Increasing traction
patency and lung volume is thought to lie in the generation of
longitudinal traction forces in the trachea.10,11 In this model, as
the lung inflates, the caudal displacement of the carina exerts a
stretching force on the trachea that is then transmitted to the upper
airway walls via the anatomical connections between the trachea
and the upper airway. This process, in effect, allows diaphragm
and rib cage muscle activity to contribute to the stability of the
upper airway during inspiration.
While animal studies have confirmed that increased caudal tracheal traction decreases measures of upper airway collapsibility
such as static closing pressures,12,13 critical collapsing pressures,14
and upper airway resistance,11 the mechanical processes linking
caudal tracheal traction forces and upper airway wall stabilization are poorly understood. Current hypotheses favor a number
of mechanisms that may operate independently or synergistically.
Both Van de Graaf10,11 and Rowley and Schwartz12,15 proposed that
longitudinal tracheal traction is transmitted to the upper airway
walls, making the upper airway resistant to collapse. These same
workers also proposed a second mechanism, whereby tracheal
traction decompresses the tissues surrounding the upper airway
resulting in a decrease in compressive tissue forces acting on upper airway walls (i.e., a reduction in transmural pressures). Other
possible mechanisms may include unfolding of the upper airway
mucosa10 and an alteration in surface forces.16
In order to examine one of these mechanisms, we measured
the effect of increasing tracheal traction on the pressure in the tissues surrounding the upper airway, or upper airway extraluminal
tissue pressure (ETP), at airway closing and reopening.
INTRODUCTION
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UPPER AIRWAY PATENCY IS KNOWN TO BE INFLUENCED
BY LUNG VOLUME. HIGHER LUNG VOLUMES ARE ASSOCIATED WITH A DECREASE IN UPPER AIRWAY resistance to airflow in awake healthy humans,1,2 and an increase in
upper airway lumen dimensions in normal subjects and obstructive sleep apnoea (OSA) patients during both wakefulness and
sleep.3-5 Thus, any sleep related reduction in lung volume may be
important in the pathogenesis of upper airway collapse in subjects
with OSA.6 In support of this, a greater respiratory disturbance
index has been shown to be related to an greater reduction in pharyngeal volume with lung volume change from total lung capacity to residual volume.7 In addition, increasing functional residual
capacity in sleeping OSA subjects has been shown to reduce the
level of continuous positive airway pressure required to keep the
upper airway patent8 and decrease OSA severity.9 Thus, reduced
lung volume may be one of the mechanisms contributing to nocturnal upper airway obstruction in OSA.
The mechanistic basis for the interaction between upper airway
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Disclosure Statement
This was not an industry supported study. Dr. Wheatley has received research support from Boehringer-Ingelheim, Pharmaxis, Cephalon, and
ResMed. Drs. Kairaitis, Byth, Parikh, Stavrinou, and Amis have indicated no
financial conflicts of interest.
Submitted for publication June 30, 2006
Accepted for publication October 24, 2006
Address correspondence to: Dr. Kristina Kairaitis, Ludwig Engel Centre for
Respiratory Research, Department of Respiratory Medicine, Westmead Hospital, Hawkesbury Rd, Westmead, NSW, Australia, 2145; Tel: (61-2) 9845
6797; Fax: (61-2) 9845 7286; E-mail: [email protected]
SLEEP, Vol. 30, No. 2, 2007
METHODS
Subjects
Studies were performed in 20 adult, supine, male, New Zealand white rabbits (2.5-3.6 kg). Other data from 7 of these rabbits
179
Tracheal Traction and ETP—Kairaitis et al
transected between the third and fourth tracheal cartilage rings.
Both the proximal and distal sections were securely cannulated,
and the animal allowed to breathe spontaneously through the caudal tracheal stump. The esophagus was isolated and tied off at the
level of the larynx.
Caudal Tracheal Traction
Graded caudal tracheal traction was applied by attaching
weights to a “string and pulley” system that exerted a caudal traction force along the cranial-caudal axis of the cranial tracheal segment via the in situ cannula. Caudal displacement of the cranial
tracheal stump was measured using a linear scale and a mark on
the string attached to the cranial tracheal stump (Figure 1).
Closing and Reopening Pressures
In 13 rabbits, the mouth was closed and a mask (sealed with
petroleum jelly) was secured over the snout. The system was leak
free to a positive air pressure of ~15cm H2O for a period of 30 s.
A 5-ml syringe was connected to the caudal end of the cranial tracheal stump and used to progressively inflate and deflate the upper airway. Separate pressure transducers (Celesco ± 200cm H2O,
IDM Instruments, Dandenong, Australia) were used to monitor
pressure inside the mask (PM) and in the cranial tracheal segment
(PUA).
Figure 1—Experimental set-up for tracheal traction. Schematic diagram of experimental setup for Protocol #1 and #2 (caudal tracheal
segment not shown). Traction was applied to the cranial segment
via a string and pulley system, to generate tracheal displacement (D,
measured from a mark on the attached string) in the same direction as the force generated by the caudal trachea. For Protocol #2,
a sealed face mask was attached to the rabbit’s snout, and a syringe
was attached to the caudal end of the cranial tracheal segment and
was used to inflate and deflate the isolated upper airway while monitoring pressure in the mask (PM) and in the distal trachea (PUA).
Dashed line drawn from the inferior nares to the tragus referenced
to the horizontal and used to define head/neck position. ETP = upper
airway extraluminal tissue pressure measured in the lateral (ETPlat)
or anterior (ETPant) pharyngeal wall.
Protocol
Two separate studies were performed. First (Protocol #1;
n=17), increasing weights (24 g each, 0 to 144 g) were applied to
the cranial tracheal segment, and the associated changes in ETP
and displacement values were measured. Each load was repeated
3 times, and the protocol was performed with the rabbit’s head
positioned at 50º to the horizontal (as referenced to a line drawn
from the tragus to the nares, Figure 1) using a specially designed
restraint which allowed flexion in the sagittal plane only.
In Protocol #2, the relationship between upper airway collapsibility, ETP, and caudal tracheal traction was examined in 13
rabbits instrumented with a snout mask (head/neck position 50º).
Quasi-static inflation and deflation of the cranial tracheal segment (air was slowly injected and withdrawn continuously at ~
0.2-1 ml/s for 5-10 runs) was used to define upper airway closing
and reopening pressures as previously described.16,18 PUA, ETPlat, and ETPant, at both closure and reopening were recorded.
Measurements were obtained with the cranial tracheal segment
unloaded and with an applied tracheal traction force of 48g.
have been reported previously elsewhere.17 The protocol was approved by the Western Sydney Area Health Service Animal Ethics
Committee.
Anesthesia
Anesthesia was induced with an intramuscular injection of ketamine (35mg/kg) and xylazine (5mg/kg), and maintained using
intravenous ketamine (15 mg/kg/hr) and xylazine (4.5 mg/kg/hr).
Measurement of ETP
Upper airway ETP was measured using pressure transducer
tipped catheters (Millar MPC 500, Millar Instruments, Houston,
Texas) surgically inserted into the tissues surrounding the pharyngeal airway as previously described.17 Briefly, the pressure transducer tip, with its sensor oriented toward the pharyngeal lumen,
was positioned within the submucosal tissues (i.e., immediately
adjacent to the pharyngeal wall), and sutured in place with a purse
string suture. Pressure was measured in the pharyngeal submucosal tissues at the level of the angle of the mandible for: 1) the right
lateral pharyngeal wall ETP (ETPlat) and 2) the anterior pharyngeal wall ETP (ETPant) at the midline in the coronal plane. Positioning of each catheter was verified via postmortem dissection at
the conclusion of each study.
Data Analysis
For Protocol #1, mean values for ETPlat and ETPant were
obtained over a steady state period of 5 seconds during the application of each weight to the cranial tracheal segment. Plots of
tracheal displacement (D) versus applied caudal traction force (F)
were developed for each individual rabbit and the data fitted with
a straight line using linear regression analysis. The slope of this
line was used to define the spring constant of the cranial tracheal
segment (Hooke’s Law: F=-kD, where k is the spring constant).
For Protocol #2, in addition to closing and reopening pressure
measurements, the upper airway transmural pressure at airway
closure and reopening for lateral and anterior ETP measurement
sites (PTMlat and PTMant, respectively) was calculated as (PUAETP). For both protocols, individual run measurements were av-
Surgery
Rabbits were studied in the supine posture. The trachea was
SLEEP, Vol. 30, No. 2, 2007
180
Tracheal Traction and ETP—Kairaitis et al
4
* * *
3
2
1
0
0
* * * * *
24 48 72 96 120 144
Tracheal traction force (g)
Figure 2—Individual rabbit data showing the effect of increasing
caudal tracheal traction on ETPlat and ETPant. Note the progressive
decrease in ETP with increasing tracheal traction force. When the
tracheal traction force is released (off), ETP returns to baseline.
Figure 3—Group mean data (± SEM) from 17 rabbits showing the
effect of increasing caudal tracheal traction force on mean ETPlat
(closed symbols) and mean ETPant (open symbols). *P<0.05 for the
corresponding ETP compared with no force.
eraged to obtain mean values for each condition. Individual rabbit
data were then pooled to obtain group mean data.
ing pressures is shown in Figure 4, Figure 5A, and Table 1. Using
the linear mixed effects model, there was a fall of 1.4 cm H2O in
both closing and reopening pressures with 48g of added tracheal
traction (P<0.001, Table 1, Figure 5A).
Statistical Analysis
For Protocol #1, the effect of increasing tracheal traction force
on mean ETPlat and ETPant in individual rabbits was examined
using a repeated measures ANOVA with Bonferroni corrected
post hoc comparisons. For Protocol #2, the effects of increasing
tracheal traction force (treated as a continuous variable) in individual rabbits (random effects) on closing and reopening pressures, ETPlat, ETPant, PTMlat, and PTMant (all treated as fixed
effects) were examined using linear mixed effects modeling.19
P<0.05 was considered significant.
Effect of Tracheal Traction Force on ETP at Closing and Reopening
Pressure
Individual data and linear mixed effects modeling for the effect of increasing tracheal traction force on ETPlat and ETPant
at closing and reopening are shown in Figure 6, Figure 5B, and
Table 1. There was a decrease of 0.2 cm H2O in ETPlat at closing
and reopening pressure with 48g of tracheal traction force (P<
0.0001 for the slope). A tracheal traction force of 48g reduced
ETPant at reopening by 0.5 cm H2O, and ETPant at closing pressure by 0.8 cm H2O (both P<0.0001 for slope, P<0.03 compared
with slope for ETPlat at both closing and reopening pressures;
Figure 5B and Table 1.
RESULTS
Protocol #1
Caudal Tracheal Traction and ETP
Effect of Tracheal Traction Force on PTM at Closing and Reopening
Pressure
Application of a caudal traction force to the cranial tracheal
segment resulted in a decrease in mean ETPlat and mean ETPant
in the majority of rabbits (Figure 2). With a tracheal traction force
of 144 g, mean ETPlat fell from 2.6 ± 0.7 cm H2O (no traction) to
2.1 ± 0.7 cm H2O, and mean ETPant fell from 1.1 ± 0.4 cm H2O
(no traction) to 0.8 ± 0.4 cm H2O (both P<0.001 compared with
no traction; Figure 3).
Individual rabbit data and linear mixed effects modeling showing the effects of increasing tracheal traction on PTMlat and PTMant are shown in Figure 7, Figure 5C, and Table 1. Using the
linear mixed effects model, there was a decrease of 0.9 cm H2O in
PTMant at reopening pressure with 48g of added tracheal traction
force (P<0.001 for the slope), but there was no change in PTMant
at closing pressure (P>0.5). However, there was a significant fall
in PTMlat at both closing and reopening pressure of 1.1 cm H2O
with 48g of tracheal traction force (P<0.0001 for slope, P<0.04
compared with slope for PTMant at both closing and reopening
pressure; Figure 5C and Table 1).
Tracheal Displacement and Spring Constants
Over the range of tracheal traction forces applied to the cranial tracheal segment, the relationship between applied force and
cranial tracheal segment displacement was linear in all rabbits
(R2>0.86). For the group, the mean (± SEM) spring constant was
0.13 ± 0.01 mm/g.
DISCUSSION
This study demonstrates that in anesthetized rabbits an increased caudal tracheal traction force is associated with both a reduction in the intraluminal pressure required to close and reopen
the upper airway and a decrease in the pressure exerted on the
upper airway walls by surrounding tissues. Moreover, the relative
changes in these pressures is such that the transmural pressure
Protocol #2
Effect of Tracheal Traction Force on Closing and Reopening Pressures
Individual rabbit data and linear mixed effect modeling for the
effect of increasing tracheal traction force on closing and reopenSLEEP, Vol. 30, No. 2, 2007
181
Tracheal Traction and ETP—Kairaitis et al
Figure 4—Individual rabbit (n=13) data (A, B) showing change (∆)
in upper airway luminal closing (A) and reopening (B) pressure with
increasing tracheal traction force Individual rabbits are represented
by different symbols. Dotted line represents no change in closing or
reopening pressures. Note that, with increasing tracheal traction force
there is a reduction in both closing and reopening pressure in the
majority of rabbits.
(difference between intraluminal and extraluminal pressures) at
which the upper airway both closes and reopens is progressively
reduced by increased caudal tracheal traction.
Figure 5—Linear mixed effects models showing the effect of tracheal traction on (A) pressure at closing (dashed line) and reopening
(solid line), (B) ETPlat at closing (dashed line) and reopening (solid
line) and ETPant at closing (dashed and dotted line) and reopening
(dotted line), and (C) PTMlat at closing (dashed line) and reopening
(solid line) and PTMant at reopening (dotted line). Data for PTMant
at closing pressure are not shown in C because there was no significant change with the addition of a caudal tracheal traction force.
All lines are significant (P<0.001). *P<0.05 for the line for the corresponding pressure at reopening, ‡P<0.05 for the line for the corresponding anterior pressure.
Critique of Methods
Anesthetized rabbits have been used in a number of physiological studies of upper airway mechanics,16,20 and we have also
previously employed this model to investigate the mechanics of
the upper airway extraluminal tissue space.17,21 The limitations of
measurement of ETP using pressure transducer tipped catheters
have been discussed previously.17 In particular, the invasive nature of the measurements mean that the change in ETP is more
useful than the absolute measurement. Although catheter tip position was confirmed at postmortem, it is possible that during tracheal traction catheters may have moved. However, since catheters were sutured to the surrounding tissues, it seems unlikely that
catheter tip position would have changed relative to surrounding
tissue structures.
For the statistical analysis, the linear mixed effects model19 was
used. This allowed comparison between the measurement sites
(anterior and lateral) and conditions (closure and reopening).
General anesthesia depresses upper airway muscle activity,22
producing a physiological model similar to sleep.23 In the present
study, upper airway muscle activity was not monitored. It is possible that during measurements of closing pressures, when negative intraluminal pressures are present, variable levels of upper
airway muscle activity, demonstrated in rabbits during ketamine/
xylazine anesthesia,24 may have influenced our findings. Indeed,
SLEEP, Vol. 30, No. 2, 2007
in some rabbits, persistent fluctuations in the ETP were seen after
the trachea had been completely sectioned (Figure 2), which suggests the possibility of ongoing upper airway muscle activity in
these rabbits.
In a manner similar to previous authors,12,13,15,25 we applied a
graded, caudally directed, external force to the isolated cranial
segment of the trachea. The only reported data describing the
magnitude of physiological caudal tracheal traction forces during
breathing are from studies in anesthetized dogs, where the force
exerted on the upper airway during a tidal inspiration was ~81
g, increasing to 250g during stimulated breathing.11 There are no
published data describing tracheal traction forces in rabbits. We
utilized a 0-144 g caudal tracheal traction force range, resulting in
up to ~20 mm of cranial tracheal segment movement. Since visual
observations in our studies suggested tracheal ring movements of
182
Tracheal Traction and ETP—Kairaitis et al
at the site of closure would directionally reflect the changes at
the exact sites of ETP measurement. Thus, transmural pressures
at the exact site of collapse is likely to have behaved in a similar
fashion to that at the ETP measurement site.
Table 1—Linear mixed effect values for ETP and transmural pressures at closing and re-opening pressure
Closing pressure
Reopening pressure
At closing pressure
ETPlat
ETPant
PTMlat
PTMant
At reopening pressure
ETPlat
ETPant
PTMlat
PTMant
Slope
(cm H2O/48g traction)
-1.4 ± 0.2
-1.4 ± 0.2
Intercept
(cm H2O)
3.1 ±1.1
8.1 ± 1.1*
-0.2±0.05‡
-0.8±0.1
-1.1±0.2‡
NS
1.4± 1.0‡
2.3 ± 0.6
1.6±1.0‡
NS
-0.2±0.05‡
-0.5±0.1*
-1.1±0.2‡
-0.9±0.3
1.5±0.7‡
2.2±0.6
6.6±1.0‡*
5.9±1.3*
Tracheal Displacement
There are no previously reported spring constant measurements for rabbit tracheae. In our study, since the cranial tracheal
segment remained attached to the larynx and pharyngeal airway,
the measured spring constant is not of the trachea alone, but rather
of the trachea in series with the laryngo-pharyngeal airway. Over
the range of traction forces (0-144g) applied, the length/force relationship for this airway was linear in all individual rabbits. This
finding suggests that tracheal traction increases longitudinal wall
tension but does not change longitudinal wall compliance (i.e.,
slope of length/force relationship is a constant).
Slope (change with tracheal traction) and intercept values (no tracheal traction) (± SEM) obtained from the linear mixed effects model for
the effect of increasing tracheal traction force on: 1) the intraluminal
pressure required to close and reopen the upper airway; 2) pressures
in the tissues in the lateral (ETPlat) and anterior (ETPant) pharyngeal
wall at reopening and closing pressure; and 3) the transmural pressure
across the lateral (PTMlat) and anterior (PTMant) pharyngeal walls
at closing and reopening pressure. See text for discussion. All values
for slopes and intercepts are significant (P<0.05). *P<0.05 compared
with at closing pressure, ‡P<0.05 compared with ETPant or PTMant.
NS = non significant
Caudal Tracheal Traction Effects on ETP
Increasing the caudal tracheal traction force resulted in a progressive decrease in mean ETPlat and ETPant. This finding suggests longitudinal forces applied to the trachea are transmitted to
the upper airway extraluminal tissue space and that the effect is
one of decompression. This finding is consistent with the model
developed by Rowley and Schwartz12,15 who hypothesized that
a reduction in ETP may be one mechanism by which the upper
airway is stabilized with increased caudal tracheal traction.
The mechanism by which tracheal traction reduces ETP is not
clear. Rowley and Schwartz12,15 describe upper airway ETP as the
sum of the radial forces acting on the the cross sectional area of
the pharynx. We have previously demonstrated that the upper airway is patent in the presence of a positive ETP.17,21 As a positive
ETP would tend to collapse the upper airway, the presence of a
patent upper airway suggests that there is an equal force opposing the collapse (i.e., an “upper airway dilator pressure”). Rowley
and Schwartz12 refer to this as the outward acting radial force.
This outward recoil force could be generated by upper airway
muscles or may be a result of the elastic properties of the upper
airway luminal wall. A reduction in ETP may imply that there has
been a reduction in the outward acting radial forces. An alternate
hypothesis for the reduction in ETP with caudal tracheal traction
centers on tissue pressure redistribution associated with caudal
movement of tissue structures, such that the volume of tissue contained within the rigid boundary formed by the bony mandible,
spinal column, and skull base is reduced.21,26,27
only a few millimeters during tidal breathing, the displacements
achieved at the maximum levels of applied force probably exceed
physiological levels for rabbits. However, our goal was to achieve
a sufficient range of tracheal traction force to clarify any resultant
effects on ETP.
For protocol #2, in which we examined the effect of tracheal
traction on the transmural pressures acting at closing and reopening pressure, we chose a force of 48g. A tracheal traction force of
48g, with a spring constant for the trachea of 0.13 mm/g is equivalent to a displacement of ~6 mm and is thus likely to encompass a
physiological level of tidal tracheal movement.
The chosen site of measurement of ETP was in the submucosal
tissues, as we have described previously.17,21 The ETP at this site
is likely to represent the sum of the forces acting on the mucosa of
the upper airway, and allows us to partition the elastic forces acting of the upper airway wall into the airway mucosa (PTM=PUAETP) and the rest of the wall components (ETP-atmospheric pressure). In their analysis of tracheal traction, Rowley et al.12 invoked
mucosal tension as a mechanism of stabilizing the upper airway.
Given that our site of measurement is submucosal, we were able
to assess this concept in a way that would not have been possible
if we had measured elsewhere in the peripharyngeal tissues. Thus,
an important outcome of our measurement site is that we were
able to assess changes in mucosal elastic properties.
In the present study, the relationship between the site at which
the upper airway closes and the pre-chosen ETP measurement
sites is not known. Since ETP is nonhomogeneous,17,21 it is possible that the measured transmural pressure was not acting at the
site of airway collapse. However, these measurements are made
under quasi-static conditions, and for the point of calculation of
transmural pressure, intraluminal pressure would be the same
throughout the airway. In addition, it is likely that ETP changes
SLEEP, Vol. 30, No. 2, 2007
Upper Airway Closing and Reopening
As has been reported by others,10,13-15 we found that increasing the tracheal traction force stabilized the upper airway, as evidenced by a decrease in both closing and reopening pressure. Previous workers have also reported that reopening pressure values
in rabbits are greater than closing pressure values.16,18 We have
previously suggested that this effect may be linked to the need
to overcome surface tension forces in the process of reopening a
closed upper airway.16 We have now demonstrated that this difference in pressures is unaffected by increasing tracheal traction
forces, suggesting that surface forces are not affected by increasing tracheal traction.
183
Tracheal Traction and ETP—Kairaitis et al
Figure 6—Individual rabbit data (n=13, A-D) showing the change from baseline in upper airway extraluminal tissue pressure in the lateral (∆ETPlat, [A, B]) and anterior (∆ETPant,[C, D]) pharyngeal wall at closing pressure (A, C) and reopening pressure (B, D) with increasing tracheal
traction force. Individual rabbits are represented by different symbols. Note that there is a reduction in both ETPlat and ETPant in the majority of
rabbits with increasing tracheal traction force.
ering of ETP was the sole explanation for the effect of tracheal
traction on upper airway closing and reopening pressures, then
increasing the tracheal traction force should not alter the PTM at
upper airway closure and reopening. This is consistent with our
data for PTMant at closing pressure. However, increased tracheal
traction was associated with a reduction in PTMlat, at both closing and reopening pressures and PTMant at reopening pressure.
This suggests that a falling ETP is not the sole explanation for the
effect of tracheal traction on airway closure and reopening.
An increase in longitudinal wall tension influences the balance of forces acting in a radial direction.30 Tuck and Remmers13
demonstrated in the passive isolated upper airway of the pig that
increasing caudal tracheal traction reduced the radial compliance
(change in cross-sectional area with intraluminal pressure) of the
hypopharynx. Thus, we might expect that an increase in longitudinal wall tension of the pharynx associated with tracheal traction would result in a reduction in the radial compliance when
measured with respect to the intraluminal pressure. Therefore, the
findings in the present study support the hypothesis of Van de
Graaf10,11 and Rowley and Schwartz12,15 that increasing tracheal
traction stabilizes the upper airway by both decreasing the pres-
ETP at Closing and Reopening Pressures
An increase in the caudal tracheal traction force was associated
with a decrease in both ETPlat and ETPant at both closing and
reopening pressure. Since ETP values are positive, a reduction in
ETP could have contributed to lowering both closing and reopening pressures. This interaction between caudal tracheal traction
force and ETP at closing and reopening pressures was greater for
ETPant than for ETPlat, implying that there may be functional tissue compartmentalization. The lateral pharyngeal wall thickness
and volume is related to the severity of OSA in humans,28,29 and
the thickness of the lateral pharyngeal walls decreases with the
application of continuous positive airway pressure.29 Thus, there
is some evidence that peripharyngeal tissue pressure distribution
may be heterogeneous in humans, consistent with tissue compartmentalization, and this may have implications for the pathogenesis of OSA.
PTM at Closing and Reopening Pressures
The upper airway PTM measurements obtained in the present
study are the first such values reported in the literature. If the lowSLEEP, Vol. 30, No. 2, 2007
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Tracheal Traction and ETP—Kairaitis et al
Figure 7—Individual rabbit data (n=13, A-D) showing the change from baseline in the upper airway transmural pressure (PUA-ETP) in the lateral
(∆PTMlat, [A, B]) and anterior pharyngeal wall (∆PTMant, [C, D]) at closing pressure (A, C) and reopening pressure (B, D) with increasing tracheal traction force. Individual rabbits are represented by different symbols. Note that in the majority of rabbits, increasing tracheal traction force
results in a reduction in the transmural pressure at both closing and reopening pressure.
sure in the tissues around the airway and by decreasing the radial
airway wall compliance. Other factors which are not measured
but which may contribute are unfolding of the upper airway mucosa and surface forces,16 and resultant increases in cross sectional
area.
ACKNOWLEDGMENTS
Supported by the National Health and Medical Research Council of Australia and the Clive and Vera Ramaciotti Foundation.
The authors would like to thank Sarah Garlick, Kylie Wilson and
Lauren Howitt for their assistance with the experimental work,
and Peter Martens for technical support.
CONCLUSION
This study reports, for the first time, the effect of caudal tracheal traction on the pressure in the tissues surrounding the upper
airway. In anesthetized rabbits, increasing caudal tracheal traction
resulted in a decrease in the pressure required to close and reopen and the upper airway, and a reduction in the pressures in the
tissues surrounding the upper airway. Increased tracheal traction
force lowered the transmural pressure at which the upper airway
both closed and reopened. These findings suggest that caudal tracheal traction acts to stabilize the upper airway by both reducing
the surrounding tissue pressure and by reducing pharyngeal wall
radial compliance. We speculate that reduction in caudal tracheal
traction may be associated with reduced lung volume during sleep
in OSA patients and may contribute to nocturnal upper airway
obstruction.
SLEEP, Vol. 30, No. 2, 2007
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