An isolated upper airway preparation in conscious dogs

The purpose of this study was to develop an isolated upper airway preparation in conscious dogs. Each of the four dogs was trained to wear an individually fitted respiratory mask and surgically prepared with two side-hole tracheostomies. After full recovery, one endotracheal tube was inserted caudally into the lower tracheostomy hole and another tube cranially into the upper tracheostomy. When the two endotracheal tubes were connected to a breathing circuit including a box-balloon system, the magnitude and pattern of the inspiratory flow through the upper airway were identical to that inhaled spontaneously into the lungs by the dogs, but the gas medium inhaled into the upper airway could be independently controlled. Thus it allowed test gas mixtures to be inhaled spontaneously through an isolated upper airway. One limitation was that the inspired gas remained in the upper airway during expiration, but this can be corrected by a simple modification of the breathing circuit. This preparation was tested in studying the respiratory effects of upper airway exposure to CO2 gas mixtures. Our results showed small but significant reduction in both rate and volume of respiration when the concentration of CO2 gas mixture inhaled through the upper airway exceeded 5%. Irregular breathing patterns were frequently elicited in these dogs by higher concentrations (greater than 12%) of CO2.     

Laryngeal influences on breathing pattern and posterior cricoarytenoid muscle activity

Receptors responding to transmural pressure, airflow, and contraction of laryngeal muscles have been previously identified in the larynx. To assess the relative contribution of these three types of receptors to the reflex changes in breathing pattern and upper airway patency, we studied diaphragmatic (DIA) and posterior cricoarytenoid muscle (PCA) activity in anesthetized dogs during spontaneous breathing and occluded efforts with and without bypassing the larynx. Inspiratory duration (TI) was longer, mean inspiratory slope (peak DIA/TI) was lower, and PCA activity was greater with upper airway occlusion than with tracheal occlusion (larynx bypassed). Bilateral section of the superior laryngeal nerves eliminated these differences. When respiratory airflow was diverted from the tracheostomy to the upper airway the only change attributable to laryngeal afferents was an increase in PCA activity. These results confirm the importance of the superior laryngeal nerves in the regulation of breathing pattern and upper airway patency and suggest a prevalent role for laryngeal negative pressure receptors.     

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.     

Expiratory flow pattern and respiratory mechanics

During resting breathing, expiration is characterized by the narrowing of the vocal folds which, by increasing the expiratory resistance, raises mean lung volume and airway pressure. This is even more pronounced in the neonatal period, during which expirations with short complete airway closure are commonly occurring. We asked to which extent differences in expiratory flow pattern may modify the inspiratory impedance of the respiratory system. To this aim, newborn puppies, piglets, and adult rats were anesthetized, paralyzed, and ventilated with different expiratory patterns, (a) no expiratory load, (b) expiratory resistive load, and (c) end-inspiratory pause. The stroke volume of the ventilator and inspiratory and expiratory times were maintained constant, and the loads were adjusted in such a way that inflation always started from the resting volume of the respiratory system. After 1 min of each ventilatory pattern, mean inspiratory impedance and compliance of lung and respiratory system were measured. The values were unchanged or minimally altered by changing the type of ventilation. We conclude that the expiratory laryngeal loading is not primarily aimed to decrease the work of breathing. It is conceivable that the expiratory pattern is oriented to increase and control mean airway pressure in the regulation of pulmonary fluid reabsorption, distribution of ventilation, and diffusion of gases.     

Blood flow in respiratory muscles during maximal exertion in ponies with laryngeal hemiplegia

The interactive effects of upper airway negative pressure and hypercapnia on the pattern of breathing were assessed in pentobarbital-anesthetized cats. At any given level of pressure in the upper airway, hypercapnia increased respiratory rate, reduced inspiratory time, and augmented tidal volume, inspiratory airflow, and the peak and rate of rise of diaphragm electrical activity. Conversely, at any given level of CO2, upper airway negative pressure decreased respiratory rate, prolonged inspiratory time, and depressed inspiratory airflow and diaphragm electromyogram (EMG) rate of rise. Application of negative pressure to the upper airway shifted the relationship between tidal volume and inspiratory time upward and rightward. The relationship between inspiratory and expiratory times, however, was linearly correlated over a wide range of chemical drives and levels of upper airway pressure. These results suggest that in the anesthetized cat upper airway negative pressure afferent inputs 1) interact in an additive fashion with hypercapnia to alter the pattern of breathing, 2) interact multiplicatively with CO2 to influence mean inspiratory airflow and diaphragm EMG rate of rise, 3) depress the generation of central inspiratory activity, 4) increase the time-dependent volume threshold for inspiratory termination, and 5) affect the ratio between inspiratory and expiratory times in a similar manner as alterations in PCO2.     

Reflex changes in tracheal smooth muscle tone during high-frequency oscillation

We examined the effect of high-frequency oscillatory ventilation (HFOV) on tracheal smooth muscle tension and upper airway resistance in anesthetized dogs. The animals were ventilated via a low tracheostomy by HFOV or conventional intermittent positive pressure ventilation (IPPV) with and without added positive end-expiratory pressure (PEEP). The transverse muscle tension of the trachea above the tracheostomy was measured and found to be lower during HFOV when compared with IPPV or IPPV with PEEP. When both vagi were cooled to 8 degrees C to interrupt afferent traffic from the lungs, there was no longer any difference between the modes of ventilation. In a second series of experiments, the airflow resistance of the upper airway above the tracheostomy was measured (Ruaw). During HFOV, Ruaw was significantly lower than during either IPPV or IPPV with PEEP. We conclude that HFOV induces a relaxation of tracheal smooth muscle and a reduction of upper airway resistance through a vagally mediated mechanism.     

Airway obstruction during periodic breathing in premature infants

To characterize changes in pulmonary resistance, timing, and respiratory drive during periodic breathing, we studied 10 healthy preterm infants (body wt 1,340 +/- 240 g, postconceptional age 35 +/- 2 wk). Periodic breathing in these infants was defined by characteristic cycles of ventilation with intervening respiratory pauses greater than or equal to 2 s. Nasal airflow was recorded with a pneumotachometer, and esophageal or pharyngeal pressure was recorded with a fluid-filled catheter. Pulmonary resistance at half-maximal tidal volume, inspiratory time (TI), expiratory time (TE), and mean inspiratory flow (VT/TI) were derived from computer analysis of five cycles of periodic breathing per infant. In 80% of infants periodic breathing was accompanied by completely obstructed breaths at the onset of ventilatory cycles; the site of airway obstruction occurred within the pharynx. The first one-third of the ventilatory phase of each cycle was accompanied by the highest airway resistance of the entire cycle (168 +/- 98 cmH2O.l-1.s). In all infants TI was greatest at the onset of the ventilatory cycle, VT/TI was maximal at the midpoint of the cycle, and TE was longest in the latter two-thirds of each cycle. A characteristic increase and subsequent decrease of 4.5 +/- 1.9 ml in end-expiratory volume also occurred within each cycle. These results demonstrate that partial or complete airway obstruction occurs during periodic breathing. Both apnea and periodic breathing share the element of upper airway instability common to premature infants.     

Posterior cricoarytenoid and diaphragm activities during tidal breathing in neonates

To investigate airflow regulation in newborn infants, we recorded airflow, volume, diaphragm (Di), and laryngeal electromyogram (EMG) during spontaneous breathing in eight supine unsedated sleeping full-term neonates. Using an esophageal catheter electrode, we recorded phasic respiratory activity consistent with that of the principal laryngeal abductors, the posterior cricoarytenoids (PCA). Sequential activation of PCA and Di preceded inspiration. PCA activity typically peaked early in inspiration followed by either a decrescendo or tonic EMG activity of variable amplitude during expiration. Expiratory airflow retardation, or braking, accompanied by expiratory prolongation and reduced ventilation, was commonly observed. In some subjects we observed a time interval between PCA onset and a sudden increase in expiratory airflow just before inspiration, suggesting that release of the brake involved an abrupt loss of antagonistic adductor activity. Our findings suggest that airflow in newborn infants is controlled throughout the breathing cycle by the coordinated action of the Di and the reciprocal action of PCA and laryngeal adductor activities. We conclude that braking mechanisms in infants interact with vagal reflex mechanisms that modulate respiratory cycle timing to influence both the dynamic maintenance of end-expiratory lung volume and ventilation.     

Reflex effects and receptor responses to upper airway pressure and flow stimuli in developing puppies

We studied the changes in breathing pattern due to pressure and airflow stimuli applied to isolated upper airway in nine 1- to 14-day-old and six 29- to 35-day-old anesthetized puppies breathing through a tracheostomy. Negative-pressure and flow, both inspiratory and expiratory, altered the breathing pattern only in the 1- to 14-day-old puppies, whereas positive pressure was ineffective in both age groups. Negative pressure caused apnea in 12% of the trials, expiratory flow in 18%, and inspiratory flow in 21%. When apnea did not occur there was a significant prolongation of inspiratory and expiratory time and a decrease of tidal volume of the first breath following the application of negative pressures. Section of the superior laryngeal nerves abolished the responses to pressure and flow. In nine 1- to 14-day-old and four 29- to 35-day-old puppies we recorded the activity of single units of the superior laryngeal nerves. We identified specialized receptors responding to pressure (68.5%), flow (2.7%), and contraction of upper airway muscles (drive, 28.8%). All types of receptors had a prevalent inspiratory-related activity. In the younger age group the discharge rate of pressure receptors at comparable negative pressures was lower than in older puppies. The strong inhibitory influences originating from the upper airway in the early stages of development presumably reflect different integrative properties of the central nervous system.     

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.     

A threshold lung volume for optimal mechanical effects on upper airway airflow dynamics: studies in an anesthetized rabbit model

Increasing lung volume improves upper airway airflow dynamics via passive mechanisms such as reducing upper airway extraluminal tissue pressures (ETP) and increasing longitudinal tension via tracheal displacement. We hypothesized a threshold lung volume for optimal mechanical effects on upper airway airflow dynamics. Seven supine, anesthetized, spontaneously breathing New Zealand White rabbits were studied. Extrathoracic pressure was altered, and lung volume change, airflow, pharyngeal pressure, ETP laterally (ETPlat) and anteriorly (ETPant), tracheal displacement, and sternohyoid muscle activity (EMG%max) monitored. Airflow dynamics were quantified via peak inspiratory airflow, flow limitation upper airway resistance, and conductance. Every 10-ml lung volume increase resulted in caudal tracheal displacement of 2.1 ± 0.4 mm (mean ± SE), decreased ETPlat by 0.7 ± 0.3 cmH(2)O, increased peak inspiratory airflow of 22.8 ± 2.6% baseline (all P < 0.02), and no significant change in ETPant or EMG%max. Flow limitation was present in most rabbits at baseline, and abolished 15.7 ± 10.5 ml above baseline. Every 10-ml lung volume decrease resulted in cranial tracheal displacement of 2.6 ± 0.4 mm, increased ETPant by 0.9 ± 0.2 cmH(2)O, ETPlat was unchanged, increased EMG%max of 11.1 ± 0.3%, and a reduction in peak inspiratory airflow of 10.8 ± 1.0%baseline (all P < 0.01). Lung volume, resistance, and conductance relationships were described by exponential functions. In conclusion, increasing lung volume displaced the trachea caudally, reduced ETP, abolished flow limitation, but had little effect on resistance or conductance, whereas decreasing lung volume resulted in cranial tracheal displacement, increased ETP and increased resistance, and reduced conductance, and flow limitation persisted despite increased muscle activity. We conclude that there is a threshold for lung volume influences on upper airway airflow dynamics.     

Upper airway cooling and l-menthol reduce ventilation in the guinea pig.

Cooling of the upper airway, which stimulates specific cold receptors and inhibits laryngeal mechanoreceptors, reduces respiratory activity in unanesthetized humans and anesthetized animals. This study shows that laryngeal cooling affects the pattern of breathing in the guinea pig and assesses the potential role of cold receptors in this response by using a specific stimulant of cold receptors (l-menthol). The response to airflows (30 ml/s, 10-s duration) through the isolated upper airway was studied in 23 anesthetized (urethan, 1 g/kg ip) guinea pigs breathing through a tracheostomy. Respiratory airflow, tidal volume, laryngeal temperature, and esophageal pressure were recorded before the challenges (control), during cold airflows (25 degrees C, 55% relative humidity), and during warm airflows (37 degrees C, saturated) with or without the addition of l-menthol. Whereas warm air trials had no effect, cold air trials, which lowered laryngeal but not nasal temperature, reduced ventilation (VE) to 85% of control, mainly by prolonging expiratory time (TE, 145% of control), an effect abolished by laryngeal anesthesia. Addition of l-menthol to the warm airflow caused a greater reduction in VE (41% of control) by prolonging TE (1,028% of control). Nasal anesthesia markedly reduced the apneogenic effect of l-menthol but did not affect the response to cold air trials. In conclusion, both cooling of the larynx and l-menthol in the laryngeal lumen reduce ventilation. Exposure of the nasal cavity to l-menthol markedly enhances this ventilatory inhibition; considering the stimulatory effect of l-menthol on cold receptors, these results suggest a predominant role of nasal cold receptors in this response.     

Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction

Positive end-expiratory pressure (PEEP) has generally been withheld from the treatment of patients with chronic airflow obstruction (CAO), in view of the risk of hyperinflation and lack of documented benefit. We studied 10 mechanically ventilated patients with exacerbated CAO and air trapping to determine the impact of PEEP on lung mechanics, alveolar pressure, and the work of breathing. PEEP levels of 5 and 10 cmH2O were applied to patients whose end-expiratory alveolar pressures were documented to be positive when breathing against ambient pressure (the auto-PEEP effect). All patients were studied under two conditions: every breath machine assisted (AMV) and every breath machine controlled (paralyzed, CMV). PEEP improved expiratory resistance without substantially increasing peak static pressure. Inspiratory resistance remained unchanged. The difference between the end-expiratory values of alveolar and central airway pressure narrowed as PEEP increased. Adding PEEP improved the effective triggering sensitivity of the ventilator, diminished ventilatory drive, and reduced the mechanical work of breathing during the machine-assisted ventilatory cycle. Our results indicate that low levels of PEEP may improve lung mechanics and reduce the effort required of mechanically ventilated patients with severe airflow obstruction, without substantially increasing the hazards of hyperinflation.     

Breathing strategy of the adult horse (Equus caballus) at rest

To investigate the mechanism underlying the polyphasic airflow pattern of the equine species, we recorded airflow, tidal volum, rib cage and abdominal motion, and the sequence of activation of the diaphragm, intercostal, and abdominal muscles during quiet breathing in nine adult horses standing at rest. In addition, esophageal, abdominal, and transdiaphragmatic pressures were simultaneously recorded using balloon-tipped catheters. Analysis of tidal flow-volume loops showed that, unlike humans, the horse at rest breathes around, rather than from, the relaxed volume of the respiratory system (Vrx). Analysis of the pattern of electromyographic activities and changes in generated pressures during the breathing cycle indicate that the first part of expiration is passive, as in humans, with deflation toward Vrx, but subsequent abdominal activity is responsible for a second phase of expiration: active deflation to below Vrx. From this end-expiratory volume, passive inflation occurs toward Vrx, followed by a second phase of inspiration: active inflation to above Vrx, brought about by inspiratory muscle contraction. Under these conditions the abdominal muscles appear to share the principal pumping duties with the diaphragm. Adoption of this breathing strategy by the horse may relate to its peculiar thoracoabdominal anatomic arrangement and to its very low passive chest wall compliance. We conclude that there is a passive and active phase to both inspiration and expiration due to the coordinated action of the respiratory pump muscles responsible for the resting adult horse's biphasic inspiratory and expiratory airflow pattern. This unique breathing pattern perhaps represents a strategy of minimizing the high elastic work of breathing in this species, at least at resting breathing frequencies.     

Regulation of end-expiratory lung volume during sleep in premature infants

To investigate the regulation of end-expiratory lung volume (EEV) in premature infants, we recorded airflow, tidal volume, diaphragm electromyogram (EMG), and chest wall displacement during sleep. In quiet sleep, EEV during breathing was 10.8 +/- 3.6 (SD) ml greater than the minimum volume reached during unobstructed apneas. In active sleep, no decrease in EEV was observed during 28 of 35 unobstructed apneas. Breaths during quiet sleep had a variable extent of expiratory airflow retardation (braking), and inspiratory interruption occurred at substantial expiratory flow rates. During active sleep, the expiratory flow-volume curve was nearly linear, proceeding nearly to the volume axis at zero flow, and diaphragm EMG activity terminated near the peak of mechanical inspiration. Expiratory duration (TE) and inspiratory duration (TI) were significantly shortened in quiet sleep vs. active sleep although tidal volume was not significantly different. In quiet sleep, diaphragmatic braking activity and shortened TE combined to maintain EEV during breathing substantially above relaxation volume. In active sleep, reduced expiratory braking and prolongation of TE resulted in an EEV that was close to relaxation volume. We conclude that breathing strategy to regulate EEV in premature infants appears to be strongly influenced by sleep state.     

Response of genioglossus muscle activity to nasal airway occlusion in normal sleeping adults

To determine the combined effect of increased subatmospheric upper airway pressure and withdrawal of phasic volume feedback from the lung on genioglossus muscle activity, the response of this muscle to intermittent nasal airway occlusion was studied in 12 normal adult males during sleep. Nasal occlusion at end expiration was achieved by inflating balloon-tipped catheters located within the portals of a nose mask. No seal was placed over the mouth. During nose breathing in non-rapid-eye-movement (NREM) sleep, nasal airway occlusion resulted in multiple respiratory efforts before arousal. Mouth breathing was not initiated until arousal. Phasic inspiratory genioglossus activity was present in eight subjects during NREM sleep. In these subjects, comparison of peak genioglossus inspiratory activity on the first three occluded efforts to the value just before occlusion showed an increase of 4.7, 16.1, and 28.0%, respectively. The relative increases in peak genioglossus activity were very similar to respective increases in peak diaphragm activity. Arousal was associated with a large burst in genioglossus activity. During airway occlusion in rapid-eye-movement (REM) sleep, mouth breathing could occur without a change in sleep state. In general, genioglossus responses to airway occlusion in REM sleep were similar in pattern to those in NREM sleep. A relatively small reflex activation of upper airway muscles associated with a sudden increase in subatmospheric pressure in the potentially collapsible segment of the upper airway may help compromise upper airway patency during sleep.     

The principle of upper airway unidirectional flow facilitates breathing in humans

Upper airway unidirectional breathing, nose in and mouth out, is used by panting dogs to facilitate heat removal via water evaporation from the respiratory system. Why some humans instinctively employ the same breathing pattern during respiratory distress is still open to question. We hypothesized that 1) humans unconsciously perform unidirectional breathing because it improves breathing efficiency, 2) such an improvement is achieved by bypassing upper airway dead space, and 3) the magnitude of the improvement is inversely proportional to the tidal volume. Four breathing patterns were performed in random order in 10 healthy volunteers first with normal breathing effort, then with variable tidal volumes: mouth in and mouth out (MMB); nose in and nose out (NNB); nose in and mouth out (NMB); and mouth in and nose out (MNB). We found that unidirectional breathing bypasses anatomical dead space and improves breathing efficiency. At tidal volumes of approximately 380 ml, the functional anatomical dead space during NMB (81 +/- 31 ml) or MNB (101 +/- 20 ml) was significantly lower than that during MMB (148 +/- 15 ml) or NNB (130 +/- 13 ml) (all P < 0.001), and the breathing efficiency obtained with NMB (78 +/- 9%) or MNB (73 +/- 6%) was significantly higher than that with MMB (61 +/- 6%) or NNB (66 +/- 3%) (all P < 0.001). The improvement in breathing efficiency increased as tidal volume decreased. Unidirectional breathing results in a significant reduction in functional anatomical dead space and improvement in breathing efficiency. We suggest this may be the reason that such a breathing pattern is preferred during respiratory distress.     

Interrupter technique for measurement of respiratory mechanics in anesthetized cats

In six spontaneously breathing anesthetized cats (pentobarbital sodium, 35 mg/kg ip), airflow, changes in lung volume, and tracheal and esophageal pressures were measured. Airflow was interrupted by brief airway occlusions during relaxed expirations (elicited via the Breuer-Hering inflation reflex) and throughout spontaneous breaths. A plateau in tracheal pressure occurred throughout relaxed expirations and the latter part of spontaneous expirations indicating respiratory muscle relaxation. Measurement of tracheal pressure, immediately preceding airflow, and corresponding volume enabled determination of respiratory system elastance and flow resistance. These were partitioned into lung and chest wall components using esophageal pressure. Respiratory system elastance was constant over the tidal volume range, divided approximately equally between the lung and chest wall. While the passive pressure-flow relationship for the respiratory system was linear, those for the lung and chest wall were curvilinear. Volume dependence of chest wall flow resistance was demonstrated. During inspiratory interruptions, tracheal pressure increased progressively; initial tracheal pressure was estimated by backward extrapolation. Inspiratory flow resistance of the lung and total respiratory system were constant. Force-velocity properties of the contracting inspiratory muscles contributed little to overall active resistance.     

Decrease in lung volume-related feedback enhances laryngeal reflexes to negative pressure.

Negative pressure applied to the upper airway has an excitatory effect on the activity of upper airway muscles and an inhibitory effect on thoracic inspiratory muscles. The role of lung volume feedback in this response was investigated in 10 anesthetized spontaneously breathing adult rabbits. To alter lung volume feedback, the lower airway was exposed to SO2 (250 ppm for 15 min), thereby blocking slowly adapting receptors (SARs). Negative pressure pulses (5, 10, and 20 cmH2O, 300-ms duration) were applied to the functionally isolated upper airway before and after SAR blockade. Tracheal airflow and electromyogram (EMG) of the genioglossus and alae nasi were recorded. Peak EMG, peak inspiratory flow, tidal volume, and respiratory timing of control breaths (3 breaths immediately preceding test) and test breaths were determined. Analysis of variance was used to determine the significance of the effects. Negative pressure pulses increased peak EMG of genioglossus and alae nasi and inspiratory duration and decreased peak inspiratory flow. These effects were larger after SAR blockade. We conclude that a decrease in volume feedback from the lung augments the response to upper airway pressure change.     

Effects of upper airway pressure on abdominal muscle activity in conscious dogs.

We have examined arousal and abdominal muscle electromyogram (EMGabd) responses to upper airway pressure stimuli during physiological sleep in four dogs with permanent side-hole tracheal stomata. The dogs were trained to sleep with a tightly fitting snout mask, hermetically sealed in place, while breathing through a cuffed endotracheal tube inserted through the tracheostomy. Sleep stage was determined by behavioral and electroencephalographic criteria. EMGabd activity was measured using bipolar fine-wire electrodes inserted into the abdominal muscle layers. Static increases or decreases in upper airway pressure (+/- 6 cmH2O), when applied at the snout mask or larynx (upper trachea), caused an immediate decrease in EMGabd on the first two to three breaths; EMGabd usually returned to control levels within the 1-min test interval. In contrast, oscillatory pressure waves at 30 Hz and +/- 3 cmH2O amplitude (or -2 to -8 cmH2O amplitude) produced an immediate and sustained reduction in IMGabd in all sleep states. Inhibition of EMGabd could be maintained over many minutes when the oscillatory pressure stimulus was pulsed by using a cycle of 0.5 s on and 0.5 s off. Oscillatory upper airway pressures were also found to be powerful arousal-promoting stimuli, producing arousal in 94% of tests in drowsiness and 66% of tests in slowwave sleep. The results demonstrate the presence of breath-by-breath upper airway control of abdominal muscle activity.