Respiratory function of hyoid muscles and hyoid arch

The position of the hyoid arch suggests that it supports soft tissue surrounding the upper airway (UA) and can act to maintain UA patency. We also suspected that muscles inserting on the hyoid arch might show respiratory patterns of activity that could be affected by respiratory stimuli. To test these possibilities, we moved the hyoid arch ventrally in six anesthetized dogs either by traction on it or by stimulation of hyoid muscles. UA resistance was decreased 73 +/- (SE) 6% and 72 +/- 6% by traction and stimulation during expiration and 57 +/- 15% and 52 +/- 8% during inspiration. Moving averages of the geniohyoid (GH) and thyrohyoid (TH) obtained in six other dogs breathing 100% O2 showed phasic respiratory activity while the sternohyoid (SH) showed phasic respiratory activity in only two of these animals and no activity in four. With progressive hypercapnia, GH and TH increased as did SH when activity was already present. Airway occlusion at end expiration augmented and prolonged inspiratory activity in the hyoid muscles but did not elicit SH activity if not already present. Occlusion at end inspiration suppressed phasic activity in hyoid muscles for as long as in the diaphragm. After vagotomy activity increased and became almost exclusively inspiratory. Activity appeared in SH when not previously present. Duration and amplitude of hyoid muscle activity were increased with negative UA pressure and augmented breaths. We conclude that the hyoid arch and muscles can strongly affect UA flow resistance. Hyoid muscles show responses to chemical, vagal, and negative pressure stimuli similar to other UA muscles.     

Chest wall motion during epidural anesthesia in dogs

To determine the relative contribution of rib cage and abdominal muscles to expiratory muscle activity during quiet breathing, we used lumbar epidural anesthesia in six pentobarbital sodium-anesthetized dogs lying supine to paralyze the abdominal muscles while leaving rib cage muscle motor function substantially intact. A high-speed X-ray scanner (Dynamic Spatial Reconstructor) provided three-dimensional images of the thorax. The contribution of expiratory muscle activity to tidal breathing was assessed by a comparison of chest wall configuration during relaxed apnea with that at end expiration. We found that expiratory muscle activity was responsible for approximately half of the changes in thoracic volume during inspiration. Paralysis of the abdominal muscles had little effect on the pattern of breathing, including the contribution of expiratory muscle activity to tidal breathing, in most dogs. We conclude that, although there is consistent phasic expiratory electrical activity in both the rib cage and the abdominal muscles of pentobarbital-anesthetized dogs lying supine, the muscles of the rib cage are mechanically the most important expiratory muscles during quiet breathing.     

Transverse abdominis length changes during eupnea, hypercapnia, and airway occlusion

The abdominal muscles accelerate airflow during expiration and may also influence the end-expiratory volume and configuration of the thorax. Although much is known about their electrical activity, the degree to which they change length during the respiratory cycle has not been previously assessed. In the present study we measured respiratory changes in transverse abdominis length using sonomicrometry in 14 pentobarbital sodium-anesthetized supine dogs and compared length changes to simultaneously recorded tidal volume and transverse abdominis electromyograms (EMG). To determine muscle resting length at passive functional residual capacity (LFRC), the animals were hyperventilated to apnea. The transverse abdominis was electrically active in all animals during resting O2 breathing (eupnea). During inspiration the transverse abdominis lengthened above resting length in all 14 dogs by a mean of 3.7 +/- 1.1% LFRC; during expiration the transverse abdominis shortened below resting length in 13 of 14 dogs by a mean of 4.2 +/- 0.9% LFRC. Increasing hyperoxic hypercapnia (produced in 9 animals) progressively heightened transverse abdominis EMG and progressively increased the extent of muscle shortening below resting length (to 12.6 +/- 3.2% LFRC at a PCO2 of 90 Torr). During single-breath airway occlusion substantial inspiratory lengthening of the transverse abdominis occurred, both during O2 breathing and during CO2 rebreathing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thoracic traction on the trachea: mechanisms and magnitude

Both inspiratory increases and tonic thoracic traction (pull of the thorax) on the trachea [Ttx(tr)] have been shown to improve patency of the upper airway. To evaluate the origins and magnitude of Ttx(tr), we studied 15 anesthetized tracheotomized dogs. We divided the midcervical trachea and attached the thoracic stub to a strain gauge. Ttx(tr), esophageal pressure, and carinal displacement were observed during various conditions. These included unobstructed and obstructed spontaneous breathing, mechanical ventilation at various levels of positive end-expiratory pressure, and progressive hypercapnic stimulation. Observations during spontaneous breathing were performed before and after vagotomy. We found that inspiratory increases in Ttx(tr) were substantial, averaging 81 +/- 8 g force and increasing to 174 +/- 22 g force at an end-expiratory CO2 concentration of 10%. Ttx(tr) did not result simply from the pull of mediastinal and pulmonary structures transmitted through the carina. Changes in intrathoracic pressure acted independently to either draw the trachea into or push the trachea out of the thorax. Thus Ttx(tr) could be explained as the sum of mediastinal traction and force generated by changes in intrathoracic pressure.     

Influence of upper airway sensory receptors on respiratory muscle activation in humans

We reasoned that neural information from upper airway (UA) sensory receptors could influence the relationship between UA and diaphragmatic neuromuscular responses to hypercapnia. In this study, the electromyographic (EMG) activities of the alae nasi (AN), genioglossus (GG), and chest wall (CW) or diaphragm (Di) to ventilatory loading were assessed in six laryngectomized, tracheostomized human subjects and in six subjects breathing with an intact UA before and after topical UA anesthesia. The EMG activities of the UA and thoracic muscles increased at similar rates with increasing hypercapnia in normal subjects, in subjects whose upper airways were anesthetized, and in laryngectomized subjects breathing with a cervical tracheostomy. Furthermore, in the laryngectomized subjects, respiratory muscle EMG activation increased with resistive inspiratory loading (15 cmH2O X l-1 X s) applied at the level of a cervical tracheostomy. At an average expired CO2 fraction of 7.0%, resistive loading resulted in a 93 +/- 26.3% (SE) increase in peak AN EMG activity, a 39 +/- 2.0% increase in peak GG EMG activity, and a 43.2 +/- 16.5% increase in peak CW (Di) EMG activity compared with control values. We conclude that the ventilatory responses of the UA and thoracic muscles to ventilatory loading are not substantially influenced by laryngectomy or UA anesthesia.     

Parasternal and external intercostal muscle shortening during eupneic breathing

The interosseous external intercostal (EI) muscles of the upper rib cage are electrically active during inspiration, but the mechanical consequence of their activation is unclear. In 16 anesthetized dogs, we simultaneously measured EI (3rd and 4th interspaces) and parasternal intercostal (PA) (3rd interspace) electromyogram and length. Muscle length was measured by sonomicrometry and expressed as a percentage of resting length (%LR). During resting breathing, each muscle was electrically active and shortened to a similar extent. Sequential EI muscle denervation (3rd and 4th interspaces) followed by PA denervation (3rd interspace) demonstrated significant reductions in the degree of inspiratory shortening for each muscle. Mean EI muscle shortening of the third and fourth interspaces decreased from -3.4 +/- 0.5 and -3.0 +/- 0.4% LR (SE) under control conditions to -0.2 +/- 0.2 and -0.8 +/- 0.3% LR, respectively, after selective denervation of each of these muscles (P less than 0.001 for each). After selective denervation of the PA muscle, its shortening decreased from -3.5 +/- 0.3 to +0.6% LR (SE) (P less than 0.001). PA muscle denervation also caused the EI muscle in the third interspace to change from inspiratory shortening of -0.2% to inspiratory lengthening of +0.2% +/- 0.2 (P less than 0.05). We conclude that during eupneic breathing 1) the EI muscles of the upper rib cage, like the PA muscles, are inspiratory agonists and actively contribute to rib cage expansion and 2) PA muscle contraction contributes to EI muscle shortening.     

Effect of positional changes of anatomic structures on upper airway dilating muscle shortening during electro- and chemostimulation.

Positional changes of anatomic structures surrounding the upper airway are known to affect pharyngeal mechanics and collapsibility. We hypothesized that these alterations also affect the ability of the upper airway dilator muscles to enlarge the pharynx by altering their ability to shorten when activated. Using sonomicrometry, we evaluated in seven anesthetized dogs the effects of changes in tracheal and head position on the length of the genioglossus (GG) and the geniohyoid (GH) and the effects of these positional changes on the magnitude of shortening of the two muscles in response to electro- (ES) and chemostimulation (CS). Caudal traction of the trachea lengthened the GG and GH in all dogs, whereas cranial displacement of the trachea and flexion of the head to a vertical position shortened the muscles. Compared with the magnitude of ES-induced shortening in the neutral position, ES-induced shortening of the GG was 144.7 +/- 14.6, 49.3 +/- 4.3, and 33.5 +/- 11.6% during caudal and cranial displacement of the trachea and during head flexion, respectively. Similar effects of the positional changes were found for the GH, as well as for both muscles during respiratory stimulation with P(CO2) of 90 Torr at the end of CO(2) rebreathing, although inspiratory muscle shortening during CS reached only one-quarter to one-third of the magnitude observed during ES. We conclude that positional alterations of anatomic structures in the neck have a dramatic effect on the magnitude of shortening of the activated GG and GH, which may reduce substantially their ability to protect pharyngeal patency.     

Inspiratory and expiratory muscle function during continuous positive airway pressure in dogs

Continuous positive airway pressure (CPAP) is known to produce activation of the expiratory muscles. Several factors may determine whether this activation can assist inspiration. In this study we asked how and to what extent expiratory muscle contraction can assist inspiration during CPAP. Respiratory muscle response to CPAP was studied in eight supine anesthetized dogs. Lung volume and diaphragmatic initial length were defended by recruitment of the expiratory muscles. At the maximum CPAP of 18 cmH2O, diaphragmatic initial lengths were longer than predicted by the passive relationship by 52 and 46% in the costal and crural diaphragmatic segments, respectively. During tidal breathing after cessation of expiratory muscle activity, a component of passive inspiration occurred before the onset of inspiratory diaphragmatic electromyogram (EMG). At CPAP of 18 cmH2O, passive inspiration represented 24% of the tidal volume (VT) and tidal breathing was within the relaxation characteristic. Diaphragmatic EMG decreased at CPAP of 18 cmH2O; however, VT and tidal shortening were unchanged. We identified passive and active components of inspiration. Passive inspiration was limited by the time between the cessation of expiratory activity and the onset of inspiratory activity. We conclude that increased expiratory activity during CPAP defends diaphragmatic initial length, assists inspiration, and preserves VT. Even though breathing appeared to be an expiratory act, there remained a significant component of active inspiratory diaphragmatic shortening, and the major portion of VT was produced during active inspiration.     

Mechanical role of expiratory muscles during breathing in prone anesthetized dogs

The purpose of the present study was to assess the mechanical role of the expiratory muscles during spontaneous breathing in prone animals. The electromyographic (EMG) activity of the triangularis sterni, the rectus abdominis, the external oblique, and the transversus abdominis was studied in 10 dogs light anesthetized with pentobarbital sodium. EMGs were recorded during spontaneous steady-state breathing in supine and prone suspended animals both before and after cervical vagotomy. We also measured the end-expiratory lung volume [functional residual capacity (FRC)] in supine and prone positions to assess the mechanical role of expiratory muscle activation in prone dogs. Spontaneous breathing in the prone posture elicited a significant recruitment of the triangularis sterni, the external oblique, and the transversus abdominis (P less than 0.05). Bilateral cervical vagotomy eliminated the postural activation of the external oblique and the transversus abdominis but not the triangularis sterni. Changes in posture during control and after cervical vagotomy were associated with an increase in FRC. However, changes in FRC, on average, were 132.3 +/- 33.8 (SE) ml larger (P less than 0.01) postvagotomy. We conclude that spontaneous breathing in prone anesthetized dogs is associated with a marked phasic expiratory recruitment of rib cage and abdominal muscles. The present data also indicate that by relaxing at end expiration the expiratory muscles of the abdominal region are directly responsible for generating roughly 40% of the tidal volume.     

Postinspiratory activity of the parasternal and external intercostal muscles in awake canines.

Previous studies have shown in awake dogs that activity in the crural diaphragm, but not in the costal diaphragm, usually persists after the end of inspiratory airflow. It has been suggested that this difference in postinspiratory activity results from greater muscle spindle content in the crural diaphragm. To evaluate the relationship between muscle spindles and postinspiratory activity, we have studied the pattern of activation of the parasternal and external intercostal muscles in the second to fourth interspaces in eight chronically implanted animals. Recordings were made on 2 or 3 successive days with the animals breathing quietly in the lateral decubitus position. The two muscles discharged in phase with inspiration, but parasternal intercostal activity usually terminated with the cessation of inspiratory flow, whereas external intercostal activity persisted for 24.7 +/- 12.3% of inspiratory time (P < 0.05). Forelimb elevation in six animals did not affect postinspiratory activity in the parasternal but prolonged postinspiratory activity in the external intercostal to 45.4 +/- 16.3% of inspiratory time (P < 0.05); in two animals, activity was still present at the onset of the next inspiratory burst. These observations support the concept that muscle spindles are an important determinant of postinspiratory activity. The absence of such activity in the parasternal intercostals and costal diaphragm also suggests that the mechanical impact of postinspiratory activity on the respiratory system is smaller than conventionally thought.     

Chest wall motion during spontaneous breathing and mechanical ventilation in dogs

We measured the volume change of the thoracic cavity (delta Vth) and the volumes displaced by the diaphragm (delta Vdi) and rib cage (delta Vrc) in six pentobarbital-anesthetized dogs lying supine. A high-speed X-ray scanner (dynamic spatial reconstructor) provided three-dimensional images of the thorax during spontaneous breathing and during mechanical ventilation with paralysis. Tidal volume (VT) was measured by integrating gas flow. Changes in thoracic liquid volume (delta Vliq, presumably caused by changes in thoracic blood volume) were calculated as delta Vth - VT. Absolute volume displaced by the rib cage was not significantly different during the two modes of ventilation. During spontaneous breathing, thoracic blood volume increased during inspiration; delta Vliq was 12.3 +/- 4.1% of delta Vth. During mechanical ventilation, delta Vliq was nearly zero. Configuration of the relaxed chest wall was similar during muscular relaxation induced by either pharmacological paralysis or hyperventilation. Expiratory muscle activity produced 50 +/- 11% of the delta Vth during spontaneous breathing. We conclude that at constant VT the volume displaced by the rib cage is remarkably similar during the transition from spontaneous breathing to mechanical ventilation, while both diaphragmatic volume displacement and changes in intrathoracic blood volume decrease by a similar amount.     

Phasic respiratory modulation of pharyngeal collapsibility via neuromuscular mechanisms in rats

Obstructive sleep apnea patients experience recurrent upper airway (UA) collapse due to decreases in the UA dilator muscle activity during sleep. In contrast, activation of UA dilators reduces pharyngeal critical pressure (Pcrit, an index of pharyngeal collapsibility), suggesting an inverse relationship between pharyngeal collapsibility and dilator activity. Since most UA muscles display phasic respiratory activity, we hypothesized that pharyngeal collapsibility is modulated by respiratory drive via neuromuscular mechanisms. Adult male Sprague-Dawley rats were anesthetized, vagotomized, and ventilated (normocapnia). In one group, integrated genioglossal activity, Pcrit, and maximal airflow (V(max)) were measured at three expiration and five inspiration time points within the breathing cycle. Pcrit was closely and inversely related to phasic genioglossal activity, with the value measured at peak inspiration being the lowest. In other groups, the variables were measured during expiration and peak inspiration, before and after each of five manipulations. Pcrit was 26% more negative (-15.0 ± 1.0 cmH(2)O, -18.9 ± 1.2 cmH(2)O; n = 23), V(max) was 7% larger (31.0 ± 1.0 ml/s, 33.2 ± 1.1 ml/s), nasal resistance was 12% bigger [0.49 ± 0.05 cmH(2)O/(ml/s), 0.59 ± 0.05 cmH(2)O/(ml/s)], and latency to induced UA closure was 14% longer (55 ± 4 ms, 63 ± 5 ms) during peak inspiration vs. expiration (all P < 0.005). The expiration-inspiration difference in Pcrit was abolished with neuromuscular blockade, hypocapnic apnea, or death but was not reduced by the superior laryngeal nerve transection or altered by tracheal displacement. Collectively, these results suggest that pharyngeal collapsibility is moment-by-moment modulated by respiratory drive and this phasic modulation requires neuromuscular mechanisms, but not the UA negative pressure reflex or tracheal displacement by phasic lung inflation.     

Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs

Respiratory muscle blood flow and organ blood flow during endotoxic shock were studied in spontaneously breathing dogs (SB, n = 6) and mechanically ventilated dogs (MV, n = 5) with radiolabeled microspheres. Shock was produced by a 5-min intravenous injection of Escherichia coli endotoxin (0.55:B5, Difco, 10 mg/kg) suspended in saline. Mean arterial blood pressure and cardiac output in the SB group dropped to 59 and 45% of control values, respectively. There was a similar reduction in arterial blood pressure and cardiac output in the MV group. Total respiratory muscle blood flow in the SB group increased significantly from the control value of 51 +/- 4 ml/min (mean +/- SE) to 101 +/- 22 ml/min at 60 min of shock. In the MV group, respiratory muscle perfusion fell from control values of 43 +/- 12 ml/min to 25 +/- 3 ml/min at 60 min of shock. In the SB group, 8.8% of the cardiac output was received by the respiratory muscle during shock in comparison with 1.9% in the MV group. In both groups of dogs, blood flow to most organs was compromised during shock; however, blood flow to the brain, gut, and skeletal muscles was higher in the MV group than in the SB group. Thus by mechanical ventilation a fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during endotoxic shock.     

Modulation of upper airway collapsibility during sleep: influence of respiratory phase and flow regimen.

We hypothesized that upper airway collapsibility is modulated dynamically throughout the respiratory cycle in sleeping humans by alterations in respiratory phase and/or airflow regimen. To test this hypothesis, critical pressures were derived from upper airway pressure-flow relationships in six tracheostomized patients with obstructive sleep apnea. Pressure-flow relationships were generated by varying the pressure at the trachea and nose during tracheostomy (inspiration and expiration) (comparison A) and nasal (inspiration only) breathing (comparison B), respectively. When a constant airflow regimen was maintained throughout the respiratory cycle (tracheostomy breathing), a small yet significant decrease in critical pressure was found at the inspiratory vs. end- and peak-expiratory time point [7.1 +/- 1.6 (SE) to 6.6 +/- 1.9 to 6.1 +/- 1.9 cmH(2)O, respectively; P < 0.05], indicating that phasic factors exerted only a modest influence on upper airway collapsibility. In contrast, we found that the inspiratory critical pressure fell markedly during nasal vs. tracheostomy breathing [1.1 +/- 1.5 (SE) vs. 6.1 +/- 1.9 cmH(2)O; P < 0.01], indicating that upper airway collapsibility is markedly influenced by differences in airflow regimen. Tracheostomy breathing was also associated with a reduction in both phasic and tonic genioglossal muscle activity during sleep. Our findings indicate that both phasic factors and airflow regimen modulate upper airway collapsibility dynamically and suggest that neuromuscular responses to alterations in airflow regimen can markedly lower upper airway collapsibility during inspiration.     

Rib cage and abdominal expiratory muscle responses to CO2 and esophageal distension

The present study compared the responses of rib cage and abdominal expiratory muscles to chemical and mechanical stimuli. In pentobarbital-anesthetized spontaneously breathing dogs, electromyograms (EMG) were recorded from the triangularis sterni (TS) and transverse abdominis (TA) muscles using bipolar intramuscular wire electrodes. During resting oxygen breathing, both muscles were electrically active during expiration. Progressive hyperoxic hypercapnia significantly augmented the expiratory activity of both the TA and the TS. However, the mean percent increases in electrical activity in response to CO2 were substantially greater for the TA than for the TS at all PCO2 levels greater than 50 Torr (P less than 0.01). Occlusion of the airway at end inspiration significantly delayed the onset of TS EMG (from 0.35 +/- 0.07 to 3.35 +/- 0.67 sec; P less than 0.002) and decreased TS EMG rate of rise (P less than 0.002), but did not significantly alter these parameters for the TA. Esophageal distension increased TS EMG in all dogs (by mean of 220 +/- 64%; P less than 0.01), but in contrast decreased TA EMG in all dogs (by a mean of 63 +/- 12%; P less than 0.001). The response to esophageal distention occurred in a graded manner and appeared to be mediated predominantly via vagal afferents. We concluded that expiratory muscles of the rib cage and abdomen manifest substantial differences in their electrical responses to chemoreceptor, pulmonary stretch receptor, and esophageal mechanoreceptor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)     

Breathing route influences upper airway muscle activity in awake normal adults

Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21-38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.     

Triangularis sterni: a primary muscle of breathing in the dog

The isolated action, pattern of neural activation, and mechanical contribution to eupnea of the triangularis sterni (transversus thoracis) muscle were studied in supine anesthetized dogs. Linear displacement transducers were used to measure the axial displacements of the ribs and sternum. Tetanic stimulation of the triangularis sterni in the apneic animal caused a marked caudal displacement of the ribs, a moderate cranial displacement of the sternum, and a decrease in lung volume. During quiet breathing, there was invariably a rhythmic activation of the muscle in phase with expiration that was independent of the presence or absence of activity in the abdominal and internal interosseous intercostal muscles. This phasic expiratory activity in the triangularis sterni was of large amplitude and caused the ribs to be more caudal and the sternum to be more cranial during the spontaneous expiratory pause than during relaxation. Additional studies on awake animals showed that rhythmic activation of the triangularis sterni occurs in all body positions and is not caused by anesthesia. These findings indicate that expiration in the dog is not a passive process and that the end-expiratory volume of the rib cage is not determined by an equilibrium of static forces alone. Rather, it is actively determined and maintained below its relaxation volume by contraction of the triangularis sterni throughout expiration. The use of this muscle is likely to facilitate inspiration by increasing the length of the parasternal intercostals and taking on a portion of their work.     

Effect of intestinal afferent stimulation on pattern of respiratory muscle activation

The purpose of the present study was to examine the reflex effects of mechanical stimulation of intestinal visceral afferents on the pattern of respiratory muscle activation. In 14 dogs anesthetized with pentobarbital sodium, electromyographic activity of the costal and crural diaphragm, parasternal intercostal, and upper airway respiratory muscles was measured during distension of the small intestine. Rib cage and abdominal motion and tidal volume were also recorded. Distension produced an immediate apnea (11.16 +/- 0.80 s). During the first postapneic breath, costal (43 +/- 7% control) and crural (64 +/- 6% control) activity were reduced (P less than 0.001). In contrast, intercostal (137 +/- 11%) and upper airway muscle activity, including alae nasi (157 +/- 16%), genioglossus (170 +/- 15%), and posterior cricoarytenoid muscles (142 +/- 7%) all increased (P less than 0.005). There was greater outward rib cage motion although the abdomen moved paradoxically inward during inspiration, resulting in a reduction in tidal volume (82 +/- 6% control) (P less than 0.005). Postvagotomy distension produced a similar apnea and subsequent reduction in costal and crural activity. However, enhancement of intercostal and upper airway muscle activation was abolished and there was a greater fall in tidal volume (65 +/- 14%). In conclusion, mechanical stimulation of intestinal afferents affects the various inspiratory muscles differently; nonvagal afferents produce an initial apnea and subsequent depression of diaphragm activity whereas vagal pathways mediate selective enhancement of intercostal and upper airway muscle activation.     

Modulation of laryngeal and respiratory pump muscle activities with upper airway pressure and flow.

The hypothesis that upper airway (UA) pressure and flow modulate respiratory muscle activity in a respiratory phase-specific fashion was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. We generated negative pressure and inspiratory flow in phase with tracheal inspiration or positive pressure and expiratory flow in phase with tracheal expiration in the isolated UA. Stimulation of UA negative pressure receptors with body temperature air resulted in a 10--15% enhancement of phasic moving-time-averaged posterior cricoarytenoid electromyographic (EMG) activity above tonic levels obtained without pressure and flow in the UA (baseline). Stimulation of UA positive pressure receptors increased phasic moving-time-averaged thyroarytenoid EMG activity above tonic levels by 45% from baseline. The same enhancement of posterior cricoarytenoid or thyroarytenoid EMG activity was observed with the addition of flow receptor stimulation with room temperature air. Tidal volume and diaphragmatic and abdominal muscle activity were unaffected by UA flow and/or pressure, whereas respiratory timing was minimally affected. We conclude that laryngeal afferents, mainly from pressure receptors, are important in modulating the respiratory activity of laryngeal muscles.     

Time of application of negative pressure pulses and upper airway muscle activity

Effect of upper airway pressure changes on thoracic inspiratory muscles has been shown to depend on the time of application during the breathing cycle. The present study was designed to investigate the importance of the time of application of upper airway negative pressure pulses on upper airway muscles. The upper airway was functionally isolated into a closed system in 24 anesthetized spontaneously breathing rabbits. Negative pressure pulses were applied in early (within the first 200 ms) and late (greater than or equal to 200 ms) inspiration, while electromyograms (EMG) of the diaphragm (Dia), genioglossus (GG), alae nasi (AN), and/or posterior cricoarytenoid (PCA) muscles were simultaneously monitored. When negative pressure pulse was applied in early inspiration, the increase in GG activity was greater [0.49 +/- 0.37 to 4.24 +/- 3.71 arbitrary units (AU)] than when negative pressure was applied in late inspiration (0.44 +/- 0.29 to 2.64 +/- 3.05 AU). Similarly, increased activation of AN (2.63 +/- 1.01 to 4.26 +/- 1.69 AU) and PCA (3.46 +/- 1.16 to 6.18 +/- 2.93 AU) was also observed with early inspiratory application of negative pressure pulses; minimal effects were seen in these muscles with late application. An inhibitory effect on respiratory timing consisting of a prolongation in inspiration (TI) and a decrease in peak Dia EMG/TI was observed as previously reported. These results indicate that the time of application of negative pressure during the breathing cycle is an important variable in determining the magnitude of the response of upper airway muscles.(ABSTRACT TRUNCATED AT 250 WORDS)