Influence of tongue muscle contraction and dynamic airway pressure on velopharyngeal volume in the rat.

The mammalian pharynx is a collapsible tube that narrows during inspiration as transmural pressure becomes negative. The velopharynx (VP), which lies posterior to the soft palate, is considered to be one of the most collapsible pharyngeal regions. I tested the hypothesis that negative transmural pressure would narrow the VP, and that electrical stimulation of extrinsic tongue muscles would reverse this effect. Pressure (-6, -3, 3, and 6 cmH2O) was applied to the isolated pharyngeal airway of anesthetized rats that were positioned in a 4.7-T MRI scanner. The volume of eight axial slices encompassing the length of the VP was computed at each level of pressure, with and without bilateral hypoglossal nerve stimulation (0.1-ms pulse, one-third maximum force, 80 Hz). Negative pressure narrowed the VP, and either whole hypoglossal nerve stimulation (coactivation of protrudor and retractor muscles) or medial nerve branch stimulation (independent activation of tongue protrudor muscles) reversed this effect, with the greatest impact in the caudal one-third of the VP. The dilating effects of medial branch stimulation were slightly larger than whole nerve stimulation. Positive pressure dilated the VP, but tongue muscle contraction did not cause further dilation under these conditions. I conclude that the narrowest and most collapsible segment of the rat pharynx is in the caudal VP, posterior to the tip of the soft palate. Either coactivation of protrudor and retractor muscles or independent contraction of protrudor muscles caused dilation of this region, but the latter was slightly more effective.     

MRI study of pharyngeal airway changes during stimulation of the hypoglossal nerve branches in rats.

The medial branch (Med) of the hypoglossal nerve innervates the tongue protrudor muscles, whereas the lateral branch (Lat) innervates tongue retractor muscles. Our previous finding that pharyngeal airflow increased during either selective Med stimulation or whole hypoglossal nerve (WHL) stimulation (coactivation of protrudor and retractor muscles) led us to examine how WHL, Med, or Lat stimulation affected tongue movements and nasopharyngeal (NP) and oropharyngeal (OP) airway volume. Electrical stimulation of either WHL, Med, or Lat nerves was performed in anesthetized, tracheotomized rats while magnetic resonance images of the NP and OP were acquired (slice thickness 0.5 mm, in-plane resolution 0.25 mm). NP and OP volume was greater during WHL and Med stimulation vs. no stimulation (P < 0.05). Ventral tongue depression (measured in the midsagittal images) and OP volume were greater during Med stimulation than during WHL stimulation (P < 0.05). Lat stimulation did not alter NP volume (P = 0.39). Our finding that either WHL or Med stimulation dilates the NP and OP airways sheds new light on the control of pharyngeal airway caliber by extrinsic tongue muscles and may lead to new treatments for patients with obstructive sleep apnea.     

Episodic hypoxia induces long-term facilitation of neural drive to tongue protrudor and retractor muscles.

Hypoxic episodes can evoke a prolonged augmentation of inspiratory motor output called long-term facilitation (LTF). Hypoglossal (XII) LTF has been assumed to represent increased tongue protrudor muscle activation and pharyngeal airway dilation. However, recent studies indicate that tongue protrudor and retractor muscles are coactivated during inspiration, a behavior that promotes upper airway patency by reducing airway compliance. These experiments tested the hypothesis that XII LTF is manifest as increased inspiratory drive to both tongue protrudor and retractor muscles. Neurograms were recorded in the medial XII nerve branch (XIIMED; contains tongue protrudor motor axons), the lateral XII nerve branch (XIILAT; contains tongue retractor motor axons), and the phrenic nerve in anesthetized, vagotomized, paralyzed, ventilated male rats. Strict isocapnia was maintained for 60 min after five 3-min hypoxic episodes (arterial Po(2) = 35 +/- 2 Torr) or sham treatment. Peak inspiratory burst amplitude showed a persistent increase in XIIMED, XIILAT, and phrenic nerves during the hour after episodic hypoxia (P < 0.05 vs. sham). This effect was present regardless of the quantification method (e.g., % baseline vs. percent maximum); however, comparisons of the relative magnitude of LTF between neurograms (e.g., XIIMED vs. XIILAT) varied with the normalization procedure. There was no persistent effect of episodic hypoxia on inspiratory burst frequency (P > 0.05 vs. sham). These data demonstrate that episodic hypoxia induces LTF of inspiratory drive to both tongue protrudor and retractor muscles and underscore the potential contribution of tongue muscle coactivation to regulation of upper airway patency.     

Fatiguing contractions of tongue protrudor and retractor muscles: influence of systemic hypoxia.

The influence of systemic hypoxia on the endurance performance of tongue protrudor and retractor muscles was examined in anesthetized, ventilated rats. Tongue protrudor (genioglossus) or retractor (hyoglossus and styloglossus) muscles were activated via medial or lateral XII nerve branch stimulation (0.1-ms pulse; 40 Hz; 330-ms trains; 1 train/s). Maximal evoked potentials (M waves) of genioglossus and hyoglossus were monitored with electromyography. Fatigue tests were performed under normoxic and hypoxic (arterial PO(2) = 50 +/- 1 Torr) conditions in separate animals. The fatigue index (FI; %initial force) after 5 min of normoxic stimulation was 85 +/- 6 and 79 +/- 7% for tongue protrudor and retractor muscles, respectively; these values were significantly lower during hypoxia (protrudor FI = 52 +/- 10, retractor FI = 18 +/- 6%; P < 0.05). Protrudor and retractor muscle M-wave amplitude declined over the course of the hypoxic fatigue test but did not change during normoxia (P < 0.05). We conclude that hypoxia attenuates tongue protrudor and retractor muscle endurance performance; potential mechanisms include neuromuscular transmission failure and/or diminished sarcolemmal excitability.     

Consequences of periodic augmented breaths on tongue muscle activities in hypoxic rats.

This study was designed to investigate the influence of hypoxia-evoked augmented breaths (ABs) on respiratory-related tongue protrudor and retractor muscle activities and inspiratory pump muscle output. Genioglossus (GG) and hyoglossus (HG) electromyogram (EMG) activities and respiratory-related tongue movements were compared with peak esophageal pressure (Pes; negative change in pressure during inspiration) and minute Pes (Pes x respiratory frequency = Pes/min) before and after ABs evoked by sustained poikilocapnic, isocapnic, and hypercapnic hypoxia in spontaneously breathing, anesthetized rats. ABs evoked by poikilocapnic and isocapnic hypoxia triggered long-lasting (duration at least 10 respiratory cycles) reductions in GG and HG EMG activities and tongue movements relative to pre-AB levels, but Pes was reduced transiently (duration of <10 respiratory cycles) after ABs. Adding 7% CO(2) to the hypoxic inspirate had no effect on the frequency of evoked ABs, but this prevented long-term declines in tongue muscle activities. Bilateral vagotomy abolished hypoxia-induced ABs and stabilized drive to the tongue muscles during each hypoxic condition. We conclude that, in the rat, hypoxia-evoked ABs 1) elicit long-lasting reductions in protrudor and retractor tongue muscle activities, 2) produce short-term declines in inspiratory pump muscle output, and 3) are mediated by vagal afferents. The more prolonged reductions in pharyngeal airway vs. pump muscle activities may lead to upper airway narrowing or collapse after spontaneous ABs.     

Anatomic consequences of intrinsic tongue muscle activation.

We recently showed respiratory-related coactivation of both extrinsic and intrinsic tongue muscles in the rat. Here, we test the hypothesis that intrinsic tongue muscles contribute importantly to changes in velopharyngeal airway volume. Spontaneously breathing anesthetized rats were placed in a MRI scanner. A catheter was placed in the hypopharynx and connected to a pressure source. Axial and sagittal images of the velopharyngeal airway were obtained, and the volume of each image was computed at airway pressures ranging from +5.0 to -5.0 cm H2O. We obtained images in the hypoglossal intact animal (i.e., coactivation of intrinsic and extrinsic tongue muscles) and after selective denervation of the intrinsic tongue muscles, with and without electrical stimulation. Denervation of the intrinsic tongue muscles reduced velopharyngeal airway volume at atmospheric and positive airway pressures. Electrical stimulation of the intact hypoglossal nerve increased velopharyngeal airway volume; however, when stimulation was repeated after selective denervation of the intrinsic tongue muscles, the increase in velopharyngeal airway volume was significantly attenuated. These findings support our working hypothesis that intrinsic tongue muscles play a critical role in modulating upper airway patency.     

Neural drive to tongue protrudor and retractor muscles following pulmonary C-fiber activation.

Hypoglossal (XII) nerve recordings indicate that pulmonary C-fiber (PCF) receptor activation reduces inspiratory bursting and triggers tonic discharge. We tested three hypotheses related to this observation: 1) PCF receptor activation inhibits inspiratory activity in XII branches innervating both tongue protrudor muscles (medial branch; XIImed) and retractor muscles (lateral branch; XIIlat); 2) reduced XII neurogram amplitude reflects decreased XII motoneuron discharge rate; and 3) tonic XII activity reflects recruitment of previously silent motoneurons. Phrenic, XIImed, and XIIlat neurograms were recorded in anesthetized, paralyzed, and ventilated rats. Capsaicin delivered to the jugular vein reduced phrenic bursting at doses of 0.625 and 1.25 mug/kg but augmented bursting at 5 mug/kg. All doses reduced inspiratory amplitude in XIImed and XIIlat (P < 0.05), and these effects were eliminated following bilateral vagotomy. Single-fiber recordings indicated that capsaicin causes individual XII motoneurons to either decrease discharge rate (n = 101/153) or become silent (n = 39/153). Capsaicin also altered temporal characteristics such that both XIImed and XIIlat inspiratory burst onset occurred after the phrenic burst (P < 0.05). Increases in tonic discharge after capsaicin were greater in XIImed vs. XIIlat (P < 0.05); single-fiber recordings indicated that tonic discharge reflected recruitment of previously silent motoneurons. We conclude that PCF receptor activation reduces inspiratory XII motoneuron discharge and transiently attenuates neural drive to both tongue protrudor and retractor muscles. However, tonic discharge appears to be selectively enhanced in tongue protrudor muscles. Accordingly, reductions in upper airway stiffness associated with reduced XII burst amplitude may be offset by enhanced tonic activity in tongue protrudor muscles.     

弥猴单侧软腭肌肉对针式电极刺激的反应

目的建立针电极口内刺激猴软腭肌肉诱发腭咽闭合运动的模式,取得软腭肌肉运动的有效刺激数值,为软腭肌肉功能重建奠定基础。方法通过解剖成年猕猴软腭的五组肌肉,确定其体表位置;利用实验动物用腭部肌肉电极定位刺激器及针式电极对软腭肌肉进行有效刺激;结合鼻咽纤维镜、头颅侧位X片及软腭造影技术观察、记录肌肉收缩及腭咽闭合动作。结果在猕猴口内定位目标肌肉进行针电极刺激可诱发肌肉收缩。刺激电压为3 V、刺激频率为20 Hz时均能诱发单侧软腭肌肉的有效收缩;单侧腭帆提肌在刺激电压为5 V、20 Hz时可发生腭咽闭合动作。咽腭肌、舌腭肌在刺激电压5 V、刺激频率100 Hz时发生软腭下降动作。腭帆张肌仅发生收缩,而未发生腭咽闭合。应用鼻咽纤维镜和X线成像技术配合能记录腭咽闭合动作。结论弥猴可作为研究软腭肌肉运动模式的实验动物。应用电极刺激软腭肌肉,可初步建立腭咽闭合的动作模式。     

Factors influencing regional patency and configuration of the human infant upper airway

To study factors influencing patency and configuration of the upper airway, we studied 11 infant cadavers using endoscopy and photography. In most cases, studies were performed shortly after death. The naso-, oro-, and hypopharynx and the larynx were studied. The upper airway was sealed at the nose and mouth so that transmural airway pressure could be raised or lowered. As pressure was lowered airway closure was seen in each of the four regions studied. With respect to closing pressure, the oropharynx was the most compliant region and the larynx the least compliant. In the naso-, oro-, and hypopharynx, lowering the transmural pressure was associated with inward movement of the anterior, posterior, and lateral airway walls. In the larynx, closure occurred by vocal cord opposition in the midline. Tension applied to the genioglossus and geniohyoid tongue muscles had an effect opposite to that of airway suction, causing a more or less symmetrical dilation of the naso- and oropharynx. When the airway was closed, additional tension was needed to produce airway reopening, suggesting that adhesion forces act to maintain airway closure. Neck flexion caused pharyngeal closure, and neck extension caused pharyngeal dilation. Secretions adherent to the walls of the airway visibly narrowed its lumen. The relevance of these findings for the obstructive sleep apnea and laryngomalacia syndromes is discussed.     

Mandible position and activation of submental and masseter muscles during sleep.

Movement of the mandible could influence pharyngeal airway caliber because the mandible is attached to the tongue and to muscles that insert on the hyoid bone. In normal subjects and patients with obstructive sleep apnea (OSA) we measured jaw position during sleep with strain gauges, as well as masseter and submental electromyograms, airflow, esophageal pressure, oximetry, electroencephalograms, and electrooculograms. Jaws of patients with OSA were open more than those of normal subjects at end expiration and opened further at end inspiration, particularly at the termination of apneas when the masseter and submental muscles contracted. Masseter activation occurred only in patients with OSA and in a pattern similar to that of submental muscles. Jaw opening at end expiration could narrow the upper airway, whereas opening at end inspiration could reflect efforts to expand the airway with tracheal tug and with submental muscle activation and efforts to open the mouth to allow mouth breathing. Masseter contraction does not close the jaw but may serve to stabilize it.     

Action of neck accessory muscles on rib cage in dogs

To investigate the action of the neck accessory muscles on the rib cage, we stimulated the sternocleidomastoid and the scalenus muscles separately in supine anesthetized dogs. Hooks screwed into the sternum and ribs were used to measure their axial displacements and the changes in anteroposterior (AP) and transverse (T) diameters of the rib cage. We found that the sternocleidomastoid and scalenus muscles, when they contract alone, cause a large axial displacement of the sternum and the ribs in a cephalad direction and expand the rib cage along both its AP and T diameters. Opening the abdomen increased the cephalad displacement of the ribs and the expansion of the lower rib cage, particularly along its T diameter, but reduced the increase in lung volume. These experiments indicate 1) that the action of the sternocleidomastoid and scalenus muscles on the rib cage is essentially the consequence of a rotation of the ribs' neck axes, resulting from the cephalad displacement of the ribs, and 2) that the fall in abdominal pressure, almost certainly by acting through the zone of apposition of the diaphragm to the rib cage, has a deflationary action on the lower rib cage, more markedly so on its lateral than its anterior wall. The experiments also suggest that the fall in abdominal pressure prevents the diaphragm from moving cephalad and aids the neck accessory muscles in inflating the lungs.     

Activation of masseter muscles with inspiratory resistance loading

Closure of the jaw exerts traction on muscles that insert on the hyoid bone and that may stabilize or expand the pharyngeal airway. We postulated that the masseter muscles, which close the jaw, would be activated when the patency of the pharyngeal airway is threatened. We therefore measured electromyographic activation of the masseters during inspiratory resistance loading and compared it with activation of chin muscles and alae nasi in 10 normal subjects. We observed no masseter activation during quiet unloaded breathing, but as pharyngeal pressure became lower there was a significant increase in masseter activation in all subjects. The change in masseter activation relative to pharyngeal pressure was similar to that of chin muscles and alae nasi. Activation of the masseter preceded the fall in pharyngeal pressure as also occurred in the chin muscles and alae nasi. We conclude that the masseters are activated by inspiratory resistance loading and have respiratory activity similar to pharyngeal airway muscles.     

Effect of geniohyoid and sternohyoid muscle contraction on upper airway resistance in the cat.

Previous investigators (van Lunteren et al. J. Appl. Physiol. 62: 582-590, 1987) have suggested that the geniohyoid and sternohyoid muscles may act as upper airway dilators in the cat. To investigate the effect of geniohyoid and sternohyoid contraction on inspiratory upper airway resistance (UAR), we studied five adult male cats anesthetized with ketamine and xylazine during spontaneous room-air breathing. Inspiratory nasal airflow was measured by sealing the lips and constructing a nose mask. Supraglottic pressure was measured using a transpharyngeal catheter placed above the larynx. Mask pressure was measured using a separate catheter. Geniohyoid and sternohyoid lengths were determined by sonomicrometry. Geniohyoid and sternohyoid contraction was stimulated by direct muscle electrical stimulation with implanted wire electrodes. Mean inspiratory UAR was determined for spontaneous breaths under three conditions: 1) baseline (no muscle stimulation), 2) geniohyoid contraction alone, and 3) sternohyoid contraction alone. Geniohyoid contraction alone produced no significant reduction in inspiratory UAR [unstimulated, 17.75 +/- 0.86 (SE) cmH2O.l-1.s; geniohyoid contraction, 19.24 +/- 1.10]. Sternohyoid contraction alone also produced no significant reduction in inspiratory UAR (unstimulated, 15.74 +/- 0.92 cmH2O.l-1.s; sternohyoid contraction, 14.78 +/- 0.78). Simultaneous contraction of the geniohyoid and sternohyoid muscles over a wide range of muscle lengths produced no consistent change in inspiratory UAR. The geniohyoid and sternohyoid muscles do not appear to function consistently as upper airway dilator muscles when UAR is used as an index of upper airway patency in the cat.     

Interaction between the canine diaphragm and intercostal muscles in lung expansion.

Changes in intrathoracic pressure produced by the various inspiratory intercostals are essentially additive, but the interaction between these muscles and the diaphragm remains uncertain. In the present study, this interaction was assessed by measuring the changes in airway opening (DeltaPao) or transpulmonary pressure (DeltaPtp) in vagotomized, phrenicotomized dogs during spontaneous inspiration (isolated intercostal contraction), during isolated rectangular or ramp stimulation of the peripheral ends of the transected C(5) phrenic nerve roots (isolated diaphragm contraction), and during spontaneous inspiration with superimposed phrenic nerve stimulation (combined diaphragm-intercostal contraction). With the endotracheal tube occluded at functional residual capacity, DeltaPao during combined diaphragm-intercostal contraction was nearly equal to the sum of the DeltaPao produced by the two muscle groups contracting individually. However, when the endotracheal tube was kept open, DeltaPtp during combined contraction was 123% of the sum of the individual DeltaPtp (P < 0.001). The increase in lung volume during combined contraction was also 109% of the sum of the individual volume increases (P < 0.02). Abdominal pressure during combined contraction was invariably lower than during isolated diaphragm contraction. It is concluded, therefore, that the canine diaphragm and intercostal muscles act synergistically during lung expansion and that this synergism is primarily due to the fact that the intercostal muscles reduce shortening of the diaphragm. When the lung is maintained at functional residual capacity, however, the synergism is obscured because the greater stiffness of the rib cage during diaphragm contraction enhances the DeltaPao produced by the isolated diaphragm and reduces the DeltaPao produced by the intercostal muscles.     

A biomechanical model of sagittal tongue bending

The human tongue is a structurally complex and extremely flexible organ. In order to better understand the mechanical basis for lingual deformations, we modeled a primitive movement of the tongue, sagittal tongue bending. We hypothesized that sagittal bending is a synergistic deformation derived from co-contraction of the longitudinalis and transversus muscles. Our model of tongue bending was based on classical bimetal strip theory, in which curvature is produced when one muscle layer contracts more so than another. Contraction was modulated via mismatched thermal expansion coefficients and temperature change (to simulate muscular contraction). Our results demonstrated that synergistic contraction produced curvature and strain results which were in better correspondence to empirical results derived from tagging MRI than were the results of contraction of the longitudinalis muscle alone. This fundamental reliance of tongue bending on the synergistic contraction of its intrinsic fibers supports the muscular hydrostat theory of tongue function.     

Computational fluid dynamics modeling of the upper airway of children with obstructive sleep apnea syndrome in steady flow

Computational fluid dynamic (CFD) analysis was used to model the effect of airway geometry on internal pressure in the upper airway of three children with obstructive sleep apnea syndrome (OSAS), and three controls. Model geometry was reconstructed from magnetic resonance images obtained during quiet tidal breathing, meshed with an unstructured grid, and solved at normative peak resting flow. The unsteady Reynolds-averaged Navier-Stokes equations were solved with steady flow boundary conditions in inspiration and expiration, using a two-equation low-Reynolds number turbulence model. Model results were validated using an in-vitro scale model, unsteady flow simulation, and reported nasal resistance measurements in children. Pharynx pressure drop strongly correlated to airway area restriction. Inspiratory pressure drop was primarily proportional to the square of flow, consistent with pressure losses due to convective acceleration caused by area restriction. On inspiration, in OSAS pressure drop occurred primarily between the choanae and the region where the adenoids overlap the tonsils (overlap region) due to airway narrowing, rather than in the nasal passages; in controls the majority of pressure drop was in the nasal passages. On expiration, in OSAS the majority of pressure drop occurred between the oropharynx (posterior to the tongue) and overlap region, and local minimum pressure in the overlap region was near atmospheric due to pressure recovery in the anterior nasopharynx. The results suggest that pharyngeal airway shape in children with OSAS significantly affects internal pressure distribution compared to nasal resistance. The model may also help explain regional dynamic airway narrowing during expiration.     

Inspiratory muscle interaction in the generation of changes in airway pressure

The mechanical interaction of the inspiratory muscles in the generation of changes in airway pressure is unclear. Using upper thoracic spinal cord stimulation to activate the intercostal muscles (IC) and bilateral supramaximal phrenic nerve stimulation to activate the diaphragm (D), we measured the changes in airway pressure produced by separate and combined IC and D activation over a wide range of lung volumes. Changes in parasternal IC and D length were assessed by sonomicrometry. With increasing lung volume, activation of the IC and D resulted in progressive decrements in generated airway pressure. Combined IC and D contraction produced greater negative swings in airway pressure than the arithmetic sum of separate IC and D contraction alone, indicating a synergistic effect. Moreover, synergism increased progressively with increasing lung volume. During combined muscle contraction, both the IC and D shortened less than during contraction of either muscle group alone. The tendency for the parasternal muscle to lengthen for a given change in airway pressure during D contraction alone increased with increasing lung volume, suggesting that the tendency for the rib cage to recoil inward increased progressively with increasing lung volume. Likewise, the tendency of the D to lengthen for a given change in airway pressure during IC contraction alone also increased progressively with increasing lung volume, suggesting that the tendency for the abdomen-D compartment to recoil inward also increased with increasing lung volume. We conclude that the IC and D interact synergistically to produce changes in airway pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of cricothyroid muscle contraction on upper airway flow dynamics in dogs.

We studied the effects of cricothyroid muscle (CT) contraction on upper airway flow dynamics in eight prone open-mouth anesthetized dogs. Animals were mechanically ventilated via a tracheostomy while a constant airflow (Vuaw) passed through the isolated upper airway. Nasal airflow (Vn) was monitored using a nasal mask and pneumotachograph. Bilateral CT contraction was induced by electrical stimulation of the external branches of the superior laryngeal nerves. During CT contraction with Vuaw of 100-443 ml/s in the inspiratory direction, total upper airway resistance (Ruaw) fell by 49.1 +/- 5.4% (SE) while supraglottic resistance fell by 63.6 +/- 3.6%; simultaneously Vn fell by 55.3 +/- 3.8% and Vuaw increased by 7.2 +/- 1.7%. Similar results were obtained when Vuaw was in the expiratory direction. In three dogs in which the attachments of the CT to either the thyroid or cricoid cartilage were severed, superior laryngeal nerve stimulation had no systematic effect on Ruaw. Because visual assessment during CT contraction consistently revealed dilation of the piriform recesses, we suggest that CT contraction is associated with pharyngeal dilation, which in open-mouth dogs (with overlapping soft palate and epiglottis) redistributes flow to the oral route with a net reduction in Ruaw. Thus the CT may have a respiratory role as a pharyngeal dilator.     

Pressure-volume behavior of the upper airway

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

Influence of passive changes of lung volume on upper airways

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.