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J Appl Physiol 92: 2236-2244, 2002. First published February 8, 2002; doi:10.1152/japplphysiol.00762.2001
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Vol. 92, Issue 6, 2236-2244, June 2002

Mechanical properties of the passive pharynx in Vietnamese pot-bellied pigs. II. Dynamics

Stephanie A. Tuck and John E. Remmers

Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

We described the dynamic mechanical properties of the passive pharynx in Vietnamese pot-bellied pigs and the effects of caudal tracheal displacement. During general anesthesia and neuromuscular blockade, airflow through the upper airway (V) and pharyngeal cross-sectional area were measured during ramp decreases in pressure downstream from the pharynx (Pdown). Measurements were made with 0, 1, and 2 cm of caudal tracheal displacement. Airflow limitation and/or negative pressure dependence (NPD) were observed in all animals. Tracheal displacement (2 cm) increased maximal V (Vmax) by 205.1 ± 105.1% (P < 0.05) relative to the value with no displacement and increased the magnitude of NPD, expressed as percent decrease in V from Vmax, from 22.9 ± 27.4 to 56.6 ± 37.5% (P < 0.05). Initial decreases in Pdown narrowed all levels of the pharynx, but, once Vmax was reached, further decreases in Pdown narrowed the hypopharynx but not the nasopharynx and oropharynx. We conclude that the hypopharynx is the flow-limiting site in the pig pharynx. Tracheal displacement not only improved airflow dynamics as Vmax increased but also resulted in pronounced NPD.

caudal tracheal displacement; sleep apnea; airflow limitation; negative-pressure dependence


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

OBSTRUCTIVE SLEEP-DISORDERED breathing (OSDB) is characterized by airflow limitation and dynamic pharyngeal collapse during inspiration. A fundamental mechanism underlying pharyngeal collapse during sleep is sleep-related decrements of pharyngeal dilator muscle activity. However, why some patients with OSDB display repeated occlusion of the pharynx and others display high upper airway (UAW) resistance is unclear. Also, little is known about the mechanical behavior of the pharynx during flow limitation and dynamic collapse. The first systematic observations of pharyngeal mechanics, including cross-sectional area (A), under dynamic conditions in people with OSDB were provided by Isono et al. (6). They investigated the interrelationships between A, driving pressure, and airflow of the hypotonic velopharynx of obstructive sleep apnea (OSA) patients. During flow limitation, a progressive decrease in A of the velopharynx was observed.

Dynamics of airflow through the UAW (V) are often interpreted by using a Starling resistor model (5, 8, 10, 13-15). Flow limitation occurs in a Starling resistor when intraluminal pressure equals the pressure external to the tube, the critical pressure (Pcrit). Experimentally, Pcrit is measured as the intraluminal pressure at the site of pharyngeal collapse when flow limitation first occurs. The flow-limiting site in this model is defined in terms of intraluminal pressure as the most downstream point where intraluminal pressure does not vary with driving pressure. Studies using the Starling resistor model have shown that maximal V (Vmax) is modulated by Pcrit as well as resistance upstream from the flow-limiting site (Rup). The Starling resistor model has provided insight into pharyngeal airflow dynamics, such as the importance of collapsibility of the flow-limiting site. This model, however, does not explain the mechanism of flow limitation, nor does it predict the geometry of the airways responsible for flow limitation.

Wave speed theory, as presented by Dawson and Elliot (2), provides a more quantitative framework for understanding the mechanics of flow limitation. This theory recognizes that collapsible tubes, such as airways, cannot carry a greater flow than the flow for which the fluid velocity equals wave speed at some point in the system. The pertinent wave speed is the speed at which a small disturbance travels in a compliant tube filled with fluid. The point in the tube at which local fluid velocity first reaches wave speed is called the "choke point." The wave speed (c) is related to the choke point area (A), the choke point area's rate of change with transmural pressure (P), and gas density (rho ).
c=(AdP<IT>/&rgr;dA</IT>)<SUP>½</SUP> (1)
Maximal flow through the tube is the product of the fluid velocity at wave speed and airway area (cA). The point where local velocity first reaches wave speed is where the product of tube area and stiffness is at a minimum. Therefore, the two characteristics determining the location of the choke point are A and wall stiffness. Unlike the Starling resistor model, wave speed theory predicts the part of the geometry of the airway responsible for flow limitation. It also provides a precisely defined rate of maximal airflow, which is determined by the local properties of the choke point.

This study investigates airflow dynamics and pharyngeal A in the isolated UAW of Vietnamese pot-bellied pigs. When obese, these animals exhibit OSDB characterized by high UAW resistance, snoring, and inspiratory flow limitation but not obstructive apneas (16). The first objective of this study was to describe the relationship between pressure, airflow, and pharyngeal A during ramps in negative pressure applied to the passive pharynx. We hypothesized that flow limitation would occur with formation of a choke point in the pharynx and that location of the choke point could be predicted from the local static mechanical properties of the pharyngeal segments described in the accompanying study (17). The second objective was to investigate the effects of caudal tracheal displacement on the dynamic mechanics of the passive pharynx. Caudal displacement of the trachea decreases pharyngeal collapsibility in the passive pig pharynx (17) as well as other preparations (10, 15) and contributes to the decrease in UAW resistance during spontaneous breathing in conjunction with inspiratory activity of pharyngeal dilator muscles (18). We hypothesized that caudal tracheal displacement would increase maximal airflow through the pharynx by stiffening and/or increasing cross-sectional area of the choke point according to Eq. 1.


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Isolated UAW preparation. Eight mature Vietnamese pot-bellied pigs were studied (5 females and 3 males). Animal characteristics are provided in Table 1 of the accompanying study (17); pig 6 from Table 1 was not included in this study. All protocols were approved by the Animal Care Committee at the University of Calgary. As described in detail in the accompanying study (17), an isolated UAW preparation was used. Briefly, during general anesthesia, the cervical trachea was transected and the animal was ventilated via the caudal trachea. A laryngeal cannula was inserted in the rostral trachea with the tip placed just rostral to the vocal cords. In contrast to the accompanying study (17), the mouth of the animal was sealed but the nose was unimpeded. The animal was paralyzed throughout the experiment by intravenous administration of pancuronium bromide (0.1 mg/kg every 15 min). Atropine (0.04 ml/kg iv) was administered as needed to minimize airway secretions.

                              
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Table 1.   Effect of tracheal displacement on Rup for individual animals

A t connector connected the laryngeal cannula to a low-impedance blower and allowed a small-diameter flexible endoscope (2.2 mm OD; model LF-P, Olympus) to be inserted into the pharynx. A rubber plug sealed between the endoscope and the t connector. The endoscope was connected to a camera (model GP-KS162, Panasonic), a monitor, and a videocassette recorder. Downstream pressure (Pdown) was measured at the laryngeal cannula by a pressure transducer (model MP-45, Validyne). A pneumotachograph (Hewlett-Packard) between the laryngeal cannula and the blower, connected to a transducer (model MP-45, Validyne), measured V.

Experimental procedures. Ramps in negative pressure lasting 12 s and reaching approximately -50 cmH2O were generated by the blower and applied to the UAW. Pharyngeal images were recorded on videotape, and V and Pdown were digitally acquired at a sampling frequency of 100 Hz by using commercial data acquisition software (DataPac, Run Technologies). A time-code generator (model VC-405, Thalner Electronics Laboratories) synchronized the videotaped images with the Pdown and V signals. Negative pressure ramps were repeated in each animal, while the nasopharynx, oropharynx, and hypopharynx were imaged at 0, 1, and 2 cm of caudal tracheal displacement as described in the accompanying study (17); under any given condition, ramps were repeated three times.

In four animals (pigs 1-4), pressure at the nasopharynx, referred to as upstream pressure (Pup), was measured. A 45-cm length of polyethylene tubing (1.57 mm ID, OD 2.08 mm OD) with side ports at the tip was inserted through the nose into the nasopharynx and connected in series to a pressure transducer (model MX-840, Medex) and a saline drip. A valve (Accuflush, Medex) between the saline source and the transducer allowed a low flow of saline (2-4 ml/h) to flush the catheter.

Data analysis. Vmax reached during the ramp and the value of Pdown at the time of Vmax were calculated for each ramp, and the mean value of the three ramps was used for analysis. Flow limitation was defined as no change in V with decreasing Pdown, and negative pressure dependence (NPD) was defined as a decrease in V with decreasing Pdown. The magnitude of NPD was expressed as the percent decrease in V from Vmax. In animals in which Pup was measured, Rup at the onset of Vmax was calculated by dividing Vmax by Pup.

Changes in pharyngeal A during the negative pressure ramps were measured by digitally capturing every 15th frame (2 images/s) of the videotaped images by using frame grabber software (SnapMagic, Quantum). The pharyngeal lumen of each digitized image was traced twice and A in pixels calculated; the mean of the two A measurements was used for analysis. To determine whether the position of the endoscope in the pharynx affected airflow dynamics, Vmax and magnitude of NPD from ramps performed with the endoscope in the nasopharynx (scope in) were compared with ramps without the endoscope or the endoscope in the larynx (scope out).

According to wave speed theory, the choke point will occur in the airway where A · dP/dA (where P is airway pressure) is at a minimum. A · dP/dA of the pharyngeal segments at the onset of flow limitation was estimated as follows: Pdown at the onset of flow limitation (Pdown at Vmax) was used as an estimate of intraluminal pressure at the choke point as airflow first became limited. A of each pharyngeal segment at Pdown at Vmax was calculated from the static A-airway pressure relationship from the accompanying study (17) and used to calculate A · dP/dA.

Statistical analysis. The effects of tracheal displacement on the dependent variables (Vmax, Pdown at Vmax, and the magnitude of NPD) were analyzed by using a repeated-measures, two-factor ANOVA. Tukey's test was used for post hoc analysis. The relationship between static and dynamic mechanics of the pharynx was analyzed by determining the strength of association between compliance (dA/dP) and closing pressure (Pclose) from the accompanying study (17) and Vmax by using Pearson product-moment correlation.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

UAW pressure-flow relationships. We hypothesized that flow limitation would occur during application of negative pressure ramps to the passive pharynx as indicated by a plateau in V with increasingly negative Pdown. Flow limitation was frequently observed, but, unexpectedly, NPD was also a common observation. Four typical patterns of V during negative pressure ramps are shown in Fig. 1. Two patterns were characterized by an increase in V to a maximal value followed by flow limitation for the remainder of the ramp (type A) or for some of the ramp followed by NPD (type B). The other two patterns were characterized by an increase in V to a maximal value followed by gradual NPD (type C) or abrupt NPD (type D). Of the ramps analyzed at 0 cm of tracheal displacement, all animals demonstrated either flow limitation or NPD; two of eight animals had flow limitation alone (type A), two NPD alone (types C and D), and four had flow limitation and NPD (type B).


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Fig. 1.   Four common patterns of airflow through the upper airway (V) during negative pressure ramps. A: type A, flow limitation. B: type B, flow limitation followed by negative pressure dependence (NPD). C: type C, NPD characterized by a gradual decrease in V. D: type D, NPD characterized by an abrupt decrease in V. Increase in V at the end of the ramp seen in types C and D is likely attributed to leaks in the isolated upper airway preparation.

Effect of endoscope placement on Vmax and magnitude of NPD. The possibility that the presence of the endoscope in the pharynx could affect airflow dynamics was investigated. In three animals, we compared the results of pressure ramps with the endoscope in the nasopharynx (scope in) and the endoscope removed or the tip of the endoscope in the larynx (scope out). Ramps performed with 2 cm of tracheal displacement applied to the UAW were compared because the magnitude of NPD was greatest during this condition (see below). In two of three animals, the magnitude of NPD was significantly less with scope in compared with scope out (P < 0.05) (Fig. 2); in one of three animals, Vmax was significantly greater with scope in compared with scope out (P < 0.05; Fig. 2). Because the presence of the endoscope in the pharynx appeared to affect airflow dynamics, only data from ramps performed without the endoscope in the pharynx, or with the endoscope in the larynx, were used for comparisons of the dependent variables (Vmax, Pdown at Vmax, magnitude of NPD).


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Fig. 2.   Effects of endoscope placement on magnitude of NPD (A) and maximal V (Vmax; B) in 3 animals. Comparisons were made between ramps performed with no endoscope or the endoscope in the larynx (scope out) and ramps performed with the endoscope in the nasopharynx (scope in) during 2 cm of caudal tracheal displacement. * Significantly different from "scope out," P < 0.05.

Effect of tracheal displacement. We hypothesized that tracheal displacement would increase Vmax. As expected, tracheal displacement significantly increased Vmax (2 vs. 0 cm of displacement, P < 0.05; Fig. 3). The Pdown at which Vmax was reached tended to decrease with tracheal displacement, although this was not statistically significant.


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Fig. 3.   Effect of caudal tracheal displacement on Vmax (A) and pressure downstream from the pharynx (Pdown) at Vmax (B). Vmax was normalized to Vmax at 0 cm of tracheal displacement. For box plots, median values are indicated by the solid horizontal line within each box. Top and bottom ends of the box are 25th and 75th percentiles, respectively; and top and bottom vertical lines are 10th and 90th percentiles, respectively. , Outliers. * Significantly different from 0 cm of tracheal displacement, P < 0.05.

To determine whether tracheal displacement affected UAW mechanics rostral to the pharynx, resistance upstream from the nasopharynx was calculated. The effect of tracheal displacement on Rup is shown in Table 1 for pigs 1-4. Tracheal displacement did not change Rup in pigs 1 and 4, whereas 2 cm of tracheal displacement significantly decreased Rup in pigs 2 and 3 compared with 0 cm of displacement. Thus tracheal displacement did not have any consistent effects on Rup of the pharynx.

The presence of pronounced NPD during negative pressure ramps was an unexpected finding as was the effect of tracheal displacement on NPD; application of caudal traction to the trachea is some animals markedly increased the fall in V from Vmax. An example of a pronounced increase in NPD with tracheal displacement in one animal is shown in Fig. 4. To determine whether tracheal displacement consistently increased the magnitude of NPD, the average change in the magnitude of NPD with 1 and 2 cm of displacement was calculated for all animals. The magnitude of NPD in all animals was significantly greater with 2 cm of tracheal displacement compared with 0 cm (magnitude of NPD was 22.9 ± 27.4, 50.0 ± 36.9, and 56.6 ± 37.5% for 0, 1, and 2 cm of tracheal displacement respectively).


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Fig. 4.   Example of the effect of caudal tracheal displacement on NPD in 1 animal. Compared with 0 cm, 1 and 2 cm of tracheal displacement increased the magnitude of NPD. Also note the increase in Vmax with caudal tracheal displacement. A: V. B: Pdown.

Pharyngeal A. Adequate images of the nasopharynx during negative pressure ramps were attained in two animals, of the oropharynx in two animals, and of the hypopharynx in three animals. Representative examples of pharyngeal A during negative pressure ramps are shown in Fig. 5. The behaviors of the nasopharynx and oropharynx were similar in that changes in A mirrored changes in V; A quickly decreased with the rapid increase in V at the beginning of the ramp, and minimum A was reached at the same time as Vmax. Once minimum A was reached, A of the nasopharynx and oropharynx either did not change or increased as Pdown continued to decrease. Thus, once Vmax was reached, the downstream pressure disturbance produced by lowering Pdown was unable to propagate to these segments, indicating that the choke point was caudal to these segments. In contrast to the nasopharynx and oropharynx, A of the hypopharynx decreased abruptly at the beginning of the ramp and continued to decrease throughout the ramp, with A approaching 0. Because the hypopharynx narrowed as Pdown decreased, even after the onset of flow limitation, the choke point was either at, or just caudal to, the hypopharynx. An example of hypopharyngeal A during pronounced NPD is shown in Fig. 6; similar to flow limitation, NPD was associated with pronounced narrowing of the hypopharynx. Nasopharyngeal and oropharyngeal A did not decrease during NPD (data not shown), suggesting that the choke point location during flow limitation and NPD were similar.


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Fig. 5.   Representative examples of changes in pharyngeal cross-sectional area (A) during ramps in negative pressure. Naso- and hypopharyngeal examples are from pig 9, and oropharyngeal example is from pig 8. B: V. C: Pdown.



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Fig. 6.   Hypopharyngeal A, V, Pdown, and endoscopic images of the hypopharynx during a negative pressure ramp with 2 cm of tracheal displacement. Pronounced narrowing of the hypopharynx occurred during NPD. Note the slitlike shape of the hypopharyngeal lumen when A is very small.

The location of the choke point in the pharynx was predicted using the static A-airway pressure relationship from the accompanying study (17). Values of A · dP/dA at the onset of flow limitation for each pharyngeal segment are shown in Fig. 7. In all cases except two, A · dP/dA was at a minimum at the hypopharynx. For most animals, tracheal displacement did not appear to alter the location of minimum A · dP/dA, although the two cases where the minimum A · dP/dA did not occur at the hypopharynx were during conditions of tracheal displacement.


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Fig. 7.   Estimated A · dP/dA (where P is airway pressure) of each pharyngeal segment for individual animals. Minimum A · dP/dA occurred at the hypopharynx most often. , No tracheal displacement; , 1 cm of tracheal displacement; black-triangle, 2 cm of tracheal displacement. Negative value of A · dP/dA occurred when Pdown at Vmax was less than the predicted closing pressure for that segment.

We expected that the dynamic behavior of the pharynx would be determined in part by the static mechanical properties of the pharyngeal segments and, in particular, the characteristics of the choke point. When Vmax was correlated with dA/dP and Pclose of the pharyngeal segments from the accompanying study (17), a negative correlation was found between Vmax and dA/dP of the hypopharynx (r2 = -0.85, P = 0.07) but not other pharyngeal segments for measurements made with 0 cm of tracheal displacement. Thus a more compliant choke point led to lower values of Vmax. No significant correlations were found between Vmax and dA/dP or Pclose measured at 2 cm of tracheal displacement for any pharyngeal segments.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

We described the dynamic mechanics of the passive pharynx in Vietnamese pot-bellied pigs by using wave speed theory as a framework. The passive pharynx exhibited flow limitation and NPD during negative pressure ramps. Both direct observation of pharyngeal A during negative pressure ramps and estimation of A · dP/dA are consistent with the choke point occurring at, or just rostral, to the hypopharynx. Application of caudal tracheal displacement to the pharynx increased Vmax, likely due to increased choke point stiffness, as predicted by wave speed theory. Interestingly, another effect of tracheal displacement was to increase the magnitude of NPD.

Methodological issues. The mouth of the animal was sealed, allowing nasopharyngeal airflow only during negative pressure ramps. Limiting airflow to the nasopharyngeal route may mimic the normal route of breathing in the intact animal because of the retropalatal configuration of the epiglottis in the pig (11). A study using a rat isolated airway preparation did report a significant difference in airflow dynamics during medial XII nerve stimulation with the oropharyngeal airway sealed compared with unsealed (5). However, these effects were attributed to differences in activation of pharyngeal musculature, and thus they may not be relevant in a paralyzed preparation.

Dynamic mechanics of the pharynx in other species have been investigated with use of similar isolated UAW preparations (5, 8, 10, 15). In these experiments, measurements of Pup were made with the catheter tip carefully positioned just rostral to the flow-limiting site. The flow-limiting site was determined as the most downstream point in the pharynx at which Pup did not vary with changes in Pdown at the onset of flow limitation; the flow-limiting site was located just rostral to the rim of the soft palate in the rat and cat. The nadir in Pup reached at the onset of flow limitation was used as a measure of Pcrit. Our Pup measurements were not made at, or just rostral to, the flow-limiting site (the hypopharynx), but rather they were made upstream from the hypopharynx at the nasopharynx. Thus our Pup measurements are not analogous to Pcrit as an additional pressure drop likely occurred across the oropharynx.

The presence of the endoscope in the pharynx during measurements may have influenced airflow dynamics because the magnitude of NPD tended to be less during ramps with the endoscope in the nasopharynx compared with ramps without the endoscope in the pharynx. Perhaps the pronounced narrowing of the hypopharynx observed during NPD was mechanically impeded by the endoscope, minimizing the decrease in V. To avoid the possible confounding effects of the endoscope, only data from ramps performed without the endoscope in the pharynx were used for comparisons of dependent variables.

Dynamic mechanics. The passive pharynx of the pig exhibited flow limitation during ramps in negative pressure. According to wave speed theory, when airflow velocity reaches wave speed (predicted by Eq. 1), the pressure disturbance, in this case a decrease in Pdown, can no longer propagate upstream and affect flow; the change in Pdown is no longer "seen" by upstream segment and flow becomes independent of, or uncouples from, Pdown. The choke point is defined by wave speed theory in terms of local properties of the tube, specifically, where A · dP/dA is at a minimum. This is equivalent to the "flow-limiting site" of the Starling resistor model, which is defined in terms of pressure: the most downstream point in the tube where intraluminal pressure does not vary with driving pressure. In this study, we used pharyngeal A instead of intraluminal pressure to determine choke point location and estimated A · dP/dA from static A-airway pressure relationships determined in the accompanying study (17).

Flow limitation in the passive pharynx of these animals was associated with narrowing of the hypopharynx but not of the oropharynx or nasopharynx. Because A is determined by intraluminal pressure, the most downstream point in the tube where A, and thus intraluminal pressure, did not vary with driving pressure was caudal to the oropharynx but not caudal to the hypopharynx. Our estimates of A · dP/dA for the three pharyngeal segments also predicts choke point formation at the hypopharynx as A · dP/dA was most often at a minimum for this segment. Therefore, the onset of flow limitation in the passive pig pharynx is associated with choke point formation at or near the hypopharynx.

Because only discrete portions of the pharynx were investigated, the choke point location cannot be precisely pinpointed within the pharynx. Also, we cannot exclude the possibility of some degree of axial movement of the choke point that may occur during flow limitation or with tracheal displacement. Because hypopharyngeal narrowing was always observed after the onset of flow limitation but never naso- or oropharyngeal narrowing, rostral migration of the choke point was likely minimal.

NPD was also a frequent feature of airflow dynamics in the passive pharynx of these animals and was associated with pronounced narrowing of the hypopharynx. NPD has been described previously in isovolume pressure-flow curves of expiratory flow (4), isolated tracheae (3), and the hypotonic human pharynx (6). However, little is known about mechanisms of NPD. Although elucidating mechanisms of NPD was not an original objective of this study, NPD was a prominent feature of airflow dynamics in this preparation and warrants speculation as to its origins.

Wave speed theory offers an explanation of NPD in collapsible tubes via the effects of longitudinal tension on choke point properties during flow limitation (19). Longitudinal tension in a tube contributes to the radial force balance if there is a curvature in the wall in the axial direction. For example, longitudinal tension in a tube with a constricted segment contributes an outward radial force acting on the tube wall at the constriction that is proportional to the magnitude of the tension and the degree of longitudinal curvature. Thus, in the presence of longitudinal tension, when flow through a tube just becomes limited and choke point area is small, the longitudinal curvature at the choke point in a tube may be large enough to cause a significant outward radial force. After the initial onset of initial flow limitation, a continued fall in Pdown can compress the tube just downstream from the constriction, reducing the curvature at the choke point. As the longitudinal curvature at the choke point is reduced, so is the magnitude of the outward radial force, decreasing choke point area, decreasing A · dP/dA, and thus decreasing wave speed, with a consequent reduction in V from Vmax .

An alternate explanation for the observed NPD could be a shift from a wave speed mechanism of flow limitation to viscous flow limitation. Viscous flow limitation results from a coupling between tube compliance and dissipative pressure losses as opposed to convective acceleration of gas in the case of wave speed flow limitation (20). Viscous flow limitation is typically associated with very small tubes, such as the peripheral airways of the lung, where the maximal flow allowed by wave speed mechanisms is larger than that allowed by viscous flow limitation. In the case of the hypopharynx, perhaps the initial onset of flow limitation was due to wave speed mechanisms, when hypopharyngeal A was relatively large. Because hypopharyngeal A became very small with continued decreases in Pdown, it may be possible that viscous flow limitation occurred with a maximal flow much lower than that due to wave speed, resulting in a fall in airflow from the initial maximal value.

Although NPD was commonly observed in this isolated UAW preparation, NPD was not a feature of airflow dynamics in the intact sleeping animal (16). Thus the pronounced NPD observed in this study may be characteristic of the passive pharynx only.

Effects of tracheal displacement. In the accompanying study, we demonstrated that caudal tracheal displacement decreased compliance of the hypopharynx in the passive pig pharynx (17). According to wave speed theory, the local properties of the choke point, the hypopharynx, determine the airflow mechanics. Equation 1 states that wave speed velocity, and thus Vmax, is determined by the area and compliance of the choke point; decreased compliance of the choke point will increase Vmax. In this study, tracheal displacement did indeed increase Vmax of the passive pharynx. These findings of increased Vmax with tracheal displacement are in agreement with studies using a feline isolated UAW preparation (10, 15).

The studies of caudal tracheal displacement using a feline isolated UAW preparation also reported increases in Rup with tracheal displacement. In our study, Rup (resistance of the airway between the nares and the nasopharynx) either decreased with tracheal displacement (2 animals) or did not change (2 animals). Why tracheal displacement would decrease nasal resistance in some animals is unclear. In the accompanying study, however, A of the nasopharynx tended to be greater with 2 vs. 0 cm of tracheal displacement, although this was not statistically significant (17). Perhaps small increases in nasopharyngeal A with tracheal displacement in some animals could account for the decreased Rup.

An interesting and unexpected finding was the increase in magnitude of NPD with caudal tracheal displacement. This effect was dramatic in some cases, with airflow decreasing by ~85% from Vmax when 2 cm of tracheal displacement were applied to the UAW compared with a decrease of ~20% in the absence of tracheal displacement (Fig. 4). Tracheal displacement would be expected to increase longitudinal tension in the airway walls, and, as discussed in the previous section, the presence of longitudinal tension in the airway walls could result in NPD. However, significant NPD was also observed in some animals with 0 cm of tracheal displacement when very little longitudinal tension in the airway walls would be expected.

Effects of luminal shape. The hypopharynx was characterized not only by pronounced decreases in A during negative pressure ramps but also by changes in luminal shape. As the hypopharynx narrowed, the lumen changed from ovoid to slitlike with the long axis in a transverse plane. Such changes in luminal shape may affect airflow dynamics through the hypopharynx independent of changes in A.

Changes in luminal shape may affect airflow dynamics by altering the amount of energy dissipation due to friction. Frictional losses associated with fluid flow through a tube depend on A of the tube but also on cross-sectional shape of the tube such that deviations from circularity are associated with greater frictional losses (1). Thus an elliptical-shaped lumen would have greater frictional losses than a circular lumen of equal A. However, energy losses due to friction depend not only on A and cross-sectional shape of the tube but also on tube length and roughness, density and viscosity of the fluid itself, velocity of fluid flow, and quality of flow (laminar or turbulent) (1). Thus the impact of luminal shape changes on airflow dynamics of the pharynx cannot be predicted without consideration of these other factors. Such an analysis would be interesting but is beyond the scope of this study.

Differences in luminal shape of the pharynx between normals and OSA patients have been acknowledged (9, 12), although the significance of this to the pathogenesis of OSA is unclear. Leiter (7) speculates that differences in luminal shape may affect the effectiveness of pharyngeal dilator muscle activity; we speculate that differences in luminal shape may also affect airflow dynamics independent of neuromuscular factors.

Relationship between static and dynamic mechanics. This study, in combination with the accompanying study (17), is unique in that both the static and dynamic mechanics of the passive pharynx were characterized in the same animals. When static compliance of the pharyngeal segments was used to predict the location of the choke point during dynamic airflow, estimated A · dP/dA was most often at a minimum at the hypopharynx. Choke point behavior of the hypopharynx was corroborated by direct observation of pharyngeal A during the negative pressure ramps. Dynamic behavior of the entire airway was related to the static mechanical properties of the choke point; as dA/dP of the hypopharynx increased, Vmax decreased. This relationship is predicted by wave speed theory because wave speed, and therefore Vmax, is inversely related to wall stiffness of the choke point (2). Thus the static mechanical properties of the individual pharyngeal segments are consistent with the dynamic behavior of the pharynx, including choke point location and effects of tracheal displacement.

In conclusion, we described the dynamic mechanical properties of the passive Vietnamese pot-bellied pig pharynx. Wave speed theory was used to predict dynamic behavior of the pharynx from static mechanical properties of the individual pharyngeal segments. In all animals, the pharynx exhibited flow limitation and/or NPD, with the hypopharynx behaving as the choke point. Stiffening the hypopharynx by application of caudal tracheal displacement increased maximal airflow through the pharynx.


    ACKNOWLEDGEMENTS

The authors acknowledge the technical assistance of Jesse Charlton.


    FOOTNOTES

Address for reprint requests and other correspondence: J. E. Remmers, Faculty of Medicine, Univ. of Calgary, 3330 Hospital Dr. NW, Calgary, AB, Canada T2N 4N1 (E-mail: jeremmer{at}ucalgary.ca).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

First published February 8, 2002;10.1152/japplphysiol.00762.2001

Received 23 July 2001; accepted in final form 4 February 2002.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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J APPL PHYSIOL 92(6):2236-2244
8750-7587/02 $5.00 Copyright © 2002 the American Physiological Society



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