Response characteristics for thermal and pressure devices commonly used for monitoring nasal and oral airflow during sleep studies.

We examined thermocouple and pressure cannulae responses to oral and nasal airflow using a polyester model of a human face, with patent nasal and oral orifices instrumented with a dual thermocouple (F-ONT2A, Grass) or a dual cannula (0588, Braebon) pressure transducer (± 10 cm H2O, Celesco) system. Tidal airflow was generated using a dual compartment facemask with pneumotachographs (Fleisch 2) connected to the model orifices. During nasal breathing: thermocouple amplitude = 0.38 Ln [pneumotachograph amplitude] + 1.31 and pressure cannula amplitude = 0.93 [pneumotachograph amplitude](2.15); during oral breathing: thermocouple amplitude = 0.44 Ln [pneumotachograph amplitude] + 1.07 and pressure cannula amplitude = 0.33 [pneumotachograph amplitude](1.72); (all range ∼ 0.1-∼ 4.0 L s(-1); r(2) > 0.7). For pneumotachograph amplitudes <1 L s(-1) (linear model) change in thermocouple amplitude/unit change in pneumotachograph amplitude was similar for nasal and oral airflow, whereas nasal pressure cannula amplitude/unit change in pneumotachograph amplitude was almost four times that for oral. Increasing oral orifice area from 0.33 cm(2) to 2.15 cm(2) increased oral thermocouple amplitude/unit change in pneumotachograph amplitude by ∼ 58% but decreased pressure cannula amplitude/unit change in pneumotachograph amplitude by 49%. For pneumotachograph amplitudes up to 1 L s(-1), alterations in inspiratory/expiratory ratios or total respiratory time did not affect the sensitivity of either nasal or oral pressure cannulae or the nasal thermocouple, but the oral thermocouple sensitivity was influenced by respiratory cycle time. Different nasal and oral responses influence the ability of these systems to quantitatively assess nasal and oral airflow and oro-nasal airflow partitioning.

Pitot-tube flowmeter for quantification of airflow during sleep.

The gold-standard pneumotachograph is not routinely used to quantify airflow during overnight polysomnography due to the size, weight, bulkiness and discomfort of the equipment that must be worn. To overcome these deficiencies that have precluded the use of a pneumotachograph in routine sleep studies, our group developed a lightweight, low dead space 'pitot flowmeter' (based on pitot-tube principle) for use during sleep. We aimed to examine the characteristics and validate the flowmeter for quantifying airflow and detecting hypopneas during polysomnography by performing a head-to-head comparison with a pneumotachograph. Four experimental paradigms were utilized to determine the technical performance characteristics and the clinical usefulness of the pitot flowmeter in a head-to-head comparison with a pneumotachograph. In each study (1-4), the pitot flowmeter was connected in series with a pneumotachograph under either static flow (flow generator inline or on a face model) or dynamic flow (subject breathing via a polyester face model or on a nasal mask) conditions. The technical characteristics of the pitot flowmeter showed that, (1) the airflow resistance ranged from 0.065 ± 0.002 to 0.279 ± 0.004 cm H(2)O L(-1) s(-1) over the airflow rates of 10 to 50 L min(-1). (2) On the polyester face model there was a linear relationship between airflow as measured by the pitot flowmeter output voltage and the calibrated pneumotachograph signal a (ß(1) = 1.08 V L(-1) s(-1); ß(0) = 2.45 V). The clinically relevant performance characteristics (hypopnea detection) showed that (3) when the pitot flowmeter was connected via a mask to the human face model, both the sensitivity and specificity for detecting a 50% decrease in peak-to-peak airflow amplitude was 99.2%. When tested in sleeping human subjects, (4) the pitot flowmeter signal displayed 94.5% sensitivity and 91.5% specificity for the detection of 50% peak-to-peak reductions in pneumotachograph-measured airflow. Our data validate the pitot flowmeter for quantification of airflow and detecting breathing reduction during polysomnographic sleep studies. We speculate that quantifying airflow during sleep can differentiate phenotypic traits related to sleep disordered breathing.

Saliva production and surface tension: influences on patency of the passive upper airway.

Pharyngeal patency is influenced by the surface tension (gamma) of the upper airway lining liquid (UAL), of which saliva is a major component. We investigated the influences of saliva production on gamma of the UAL, and upper airway re-opening and closing pressures. In 10 supine, male, anaesthetized, tracheostomised, mechanically ventilated New Zealand White rabbits, we measured re-opening and closing of the passive isolated upper airway at baseline and following graded (cumulative) doses of methacholine or atropine. Upper airway liquid volume index (UALVI) was assessed using a standardized suction procedure (secretion weight obtained per second) expressed as the natural logarithm (LnUALVI). The gamma of UAL samples were measured using the 'pull-off' force technique. Across all animals, baseline values were: LnUALVI -6.2 (-8.6 to -5.4) median (interquartile range), gamma of UAL 58.9 (56.6-59.9) mN m(-1), re-opening 8.6 (6.9-11.1) cmH(2)O, and closing pressures 3.2 (1.8-5.7) cmH(2)O. LnUALVI increased by approximately 0.17 per microg kg(-1) methacholine and decreased by approximately 0.14 per 100 microg kg(-1) atropine (both P < 0.03, linear mixed effects modelling). Surface tension was unchanged by methacholine but increased by approximately 0.6 mN m(-1) per 100 microg kg(-1) atropine (P < 0.004). When data were analysed across all animals, both re-opening and closing pressures increased as surface tension increased (by approximately 0.4 cmH(2)O mN(-1) and by approximately 0.7 cmH(2)O mN(-1), respectively; both P < 0.05). We conclude that saliva production influences upper airway mechanical properties partly via alterations in gamma of UAL. We speculate that in obstructive sleep apnoea, altered autonomic activity may reduce saliva production and increase surface tension of the upper airway lining liquid, thus increasing the likelihood of upper airway obstruction.

Initiating oral breathing in response to nasal loading: asthmatics versus healthy subjects.

Factors influencing nasal versus oral breathing in asthmatics are not well understood. The current authors hypothesised that asthmatic subjects have enhanced perception of nasal threshold loads, and switch from nasal to oral breathing at a lower load than healthy subjects. In total, 15 mild asthmatic and 20 healthy control subjects breathed nasally via an inspiratory threshold loading device. Nasal loading was progressively increased until subjects switched to oral breathing. Load perception at switching was rated using a Borg scale. Nasal resistance was measured using posterior rhinomanometry. The protocol was repeated before and after nasal decongestant administration in subgroups of 10 healthy control and six asthmatic subjects. Inspiratory nasal resistance was within normal limits for most subjects and was not significantly different between asthmatics and healthy controls. Compared with controls, asthmatics switched to oral breathing at a significantly lower nasal load but rated "difficulty breathing in" at the same level. Decongestant significantly lowered nasal resistance but did not change the nasal load initiating switching in either subgroup. Enhanced perception of nasal loading may trigger increased oral breathing in asthmatics, potentially enhancing exposure to nonconditioned inhaled gas and contributing to the occurrence and/or severity of bronchoconstrictive exacerbations.

Older individuals have increased oro-nasal breathing during sleep.

Breathing route during sleep has been studied very little, however, it has potential importance in the pathophysiology of sleep disordered breathing. Using overnight polysomnography, with separate nasal and oral thermocouple probes, data were obtained from 41 subjects (snorers and nonsnorers; 25 male and 16 female; aged 20-66 yrs). Awake, upright, inspiratory nasal resistance (Rn) was measured using posterior rhinomanometry. Each 30-s sleep epoch (not affected by apnoeas/hypopnoeas) was scored for presence of nasal and/or oral breathing. Overnight, seven subjects breathed nasally, one subject oro-nasally and the remainder switched between nasal and oro-nasal breathing. Oral-only breathing rarely occurred. Nasal breathing epochs were 55.79 (69.78) per cent of total sleep epochs (%TSE; median (interquartile range)), a value not significantly different to that for oro-nasal (TSE: 44.21 (68.66)%). Oro-nasal breathing was not related to snoring, sleep stage, posture, body mass index, height, weight, Rn (2.19 (1.77) cm H2O x L(-1) x sec(-1)) or sex, but was positively associated with age. Subjects > or = 40 yrs were approximately six times more likely than younger subjects to spend >50% of sleep epochs utilising oro-nasal breathing. Ageing is associated with an increasing occurrence of oro-nasal breathing during sleep.

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Nasal resistance and flow resistive work of nasal breathing during exercise: effects of a nasal dilator strip.

Using posterior rhinomanometry, we measured nasal airflow resistance (Rn) and flow-resistive work of nasal breathing (WONB), with an external nasal dilator strip (ENDS) and without (control), in 15 healthy adults (6 men, 9 women) during exclusive nasal breathing and graded (50-230 W) exercise on a cycle ergometer. ENDS decreased resting inspiratory and/or expiratory Rn (at 0.4 l/s) by >0.5 cmH(2)O. l(-1). s in 11 subjects ("responders"). Inspired ventilation (VI) increased with external work rate, but tended to be greater with ENDS. Inspiratory and expiratory Rn (at 0.4 l/s) decreased as VI increased but, in responders, tended to remain lower with ENDS. Inspiratory (but not expiratory) Rn at peak nasal airflow (Vn) increased as VI increased but, again, was lower with ENDS. At a VI of approximately 35 l/min, ENDS decreased flow limitation and hysteresis of the inspiratory transnasal pressure-flow curve. In responders, ENDS reduced inspiratory WONB per breath and inspiratory nasal power values during exercise. We conclude that ENDS stiffens the lateral nasal vestibule walls and, in responders, may reduce the energy required for nasal ventilation during exercise.

Nasal airflow dynamics: mechanisms and responses associated with an external nasal dilator strip.

The adhesive external nasal dilator strip (ENDS) is widely advocated for prevention of snoring and promotion of nasal breathing during exercise. In the present study, the effects of the ENDS on nasal airflow resistance (Rn) in normal subjects were examined and factors determining individual responses to the ENDS explored. Using posterior rhinomanometry, 20 healthy Caucasian adults (10 males, 10 females; age: 18-56 yrs) were studied during quiet tidal breathing and voluntary hyperpnoea with (ENDS) and without (control) ENDS and with a placebo strip (placebo) before and after application of a topical nasal decongestant (oxymetazoline hydrochloride). During tidal breathing, only nine subjects showed a significantly (p<0.05) decreased inspiratory and/or expiratory Rn with the ENDS ("responders"). During the control, inspiratory Rn (at 0.4 L x s(-1)) was higher in "responders" than "nonresponders" (3.28+/-0.16 versus 2.60+/-0.08 cmH2O x L(-1) x s; p=0.04). The effects of nasal decongestant and the ENDS were additive. During voluntary hyperpnoea, inspiratory Rn (at 1.0 L x s(-1)) and the hysteresis of the inspiratory transnasal pressure/flow curve were decreased with the ENDS in most subjects. It is concluded that the external nasal dilator strip influences nasal airflow dynamics by both dilation of the nasal valve and stabilization of the lateral nasal vestibule walls and may be more effective in subjects with a high resting nasal airflow resistance.

Influence of intra-oral maxillary sports mouthguards on the airflow dynamics of oral breathing.

PURPOSE: Mouthguards worn during sporting competition may influence oral airway flow dynamics and potentially increase airflow resistance during mouth breathing. METHODS: We measured oral airflow resistance (RO) in 10 normal subjects (four men, six women, age 29 +/- 3 yr, mean +/- SEM) wearing two different custom-made maxillary mouthguards. RESULTS: During tidal mouthpiece breathing (jaw position controlled), inspiratory R(O) (at (1.4 L x s(-1)) increased from 0.22 (0.15-0.46) cm H2O x L(-1) x s(-1) (median and interquartile range) to 0.47 (0.24-0.52) cm H2O x L(-1) x s(-1) with mouthguard 1 (general sports mouthguard) and from 0.34 (0.27-0.51) to 0.46 (0.39-0.86) cm H2O x L(-1) x s(-1) (N = 8) with mouthguard 2 (laminated, field hockey mouthguard, both P < 0.05). With oral only mask breathing (jaw position not controlled), inspiratory R(O) (at 0.4 L x s(-1)) increased to 1.02 (0.42-1.57) cm H2O x L(-1) x s(-1) (P < 0.03, compared with mouthpiece) but was variably affected by both mouthguards. At 1.0 L x s(-1), there was a tendency for both mouthguards to increase inspiratory R(O); however, this effect only reached significance for mouthguard 1 during mouthpiece breathing. CONCLUSION: Thus, although maxillary mouthguards do increase R(O) when jaw position is controlled, individual subjects respond differently when in control of mouth opening. This may be related to variable recruitment of compensatory mechanisms (e.g. mouth opening and/or oral airway dilator muscle activity).

Route of breathing in patients with asthma.

STUDY OBJECTIVES: To measure route of breathing in chronic asthmatic patients during and after an acute severe exacerbation. PATIENTS OR PARTICIPANTS: Thirteen asthmatic patients were studied during hospital admission for acute asthma and, in 9 patients, again when asymptomatic. Nine healthy subjects were also studied. INTERVENTIONS: Spontaneous route of breathing was qualitatively assessed using oral and nasal thermistor probes, and was then quantified using a dual compartment face mask with attached pneumotachographs. MEASUREMENTS AND RESULTS: All asthmatic patients had severe bronchoconstriction initially (FEV(1), 46 +/- 3% of predicted) that had resolved at follow-up (FEV(1), 91 +/- 6% of predicted). No healthy subject had evidence of bronchoconstriction (FEV(1), 102 +/- 5% of predicted). During acute asthma, 11 asthmatics were spontaneously breathing oronasally, as assessed using thermistor probes, while all 13 breathed oronasally via face mask. When assessed using thermistor probes, seven of nine asymptomatic asthmatic patients studied were breathing exclusively via the nose; however, all breathed oronasally via face mask. In contrast, while eight of nine healthy subjects were also breathing exclusively via the nose when assessed using thermistor probes, all breathed nasally only via face mask. CONCLUSIONS: Thus, when asymptomatic and at rest, asthmatic patients breathe exclusively via the nose. However, during acute exacerbations of asthma, these patients switch to oronasal breathing. Unlike healthy subjects, chronic asthmatic patients also switch to oronasal breathing when wearing a face mask, irrespective of the degree of bronchoconstriction. We speculate that asthmatics may have an increased tendency to switch to oral breathing, a factor that may contribute to the pathogenesis of their asthma.

Nasal dilator strips increase maximum inspiratory flow via nasal wall stabilization.

OBJECTIVE: Inspiratory flow limitation associated with collapse of the nasal vestibular walls is a feature of nasal breathing at high ventilatory levels. We examined whether an external nasal dilator strip (ENDS) device (Breathe Right, CNS Inc., Chanhassen, MN) influences maximum inspiratory and expiratory flow rates. STUDY DESIGN: Prospective, randomized. METHODS: We studied 20 Caucasian subjects (13 female, 7 male; age range, 16-49 y) performing maximum-effort nasal flow-volume loop studies with (ENDS) and without ENDS (control) and following topical nasal decongestant (oxymetazoline hydrochloride, 0.2 mg per nostril). RESULTS: ENDS increased peak inspiratory flow from 2.55+/-0.24 L/s (mean+/-standard error [SE]) to 2.86+/-0.25 L/s and forced inspiratory flow at 50% of vital capacity from 2.23+/-0.24 L/s to 2.53+/-0.24 L/s (both, P<.0001), but had no effect on maximum expiratory flows. Nasal decongestant increased the forced expiratory volume in 1 second from 3.39+/-0.22 L/s to 3.59+/-0.22 L/s and the average forced expiratory flow over 25% to 75% of vital capacity from 3.31+/-0.31 L/s to 3.61+/-0.28 L/s (both, P< or = .008), but had no effect on maximum inspiratory flows. The combination of decongestant and ENDS increased both inspiratory and expiratory maximum flows. CONCLUSION: Since ENDS selectively increases maximum nasal inspiratory flow rates, we conclude that ENDS increases inspiratory nasal patency during maximum inspiratory efforts through the nose by supporting the lateral nasal vestibular walls and making them more resistant to collapse.

Nasal vestibule wall elasticity: interactions with a nasal dilator strip.

We studied the effect of an adhesive external nasal dilator strip (ENDS) on external nasal geometry in 20 healthy Caucasian adults (10 men, 10 women; age 21-45 yr). The recoil force exerted by ENDS was estimated by bending the device (n = 10) with known weights. In the horizontal direction, a small/medium-sized ENDS in situ exerted a unilateral recoil force of 21.4-22.6 g. Application of ENDS resulted in a displacement of the lateral nasal vestibule walls that had both anterosuperior and horizontal components and that was maintained over an 8-h period. The resultant unilateral nasal vestibule wall displacement at the tip of the device was at 47.6 +/- 2.0 degrees to the horizontal (as related to the plane of the device when in situ) and had a magnitude of 3.5 +/- 0.1 mm. ENDS increased external nasal cross-sectional area by 23.0-65.3 mm2. Nasal vestibule wall compliance was estimated at 0.05-0.16 mm/g. Thus ENDS applies a relatively constant abducting force irrespective of nasal width. Variable responsiveness to ENDS may be related to differences in elastic properties of the nasal vestibule wall.

Oral airway resistance during wakefulness in patients with obstructive sleep apnoea.

BACKGROUND: Patients with obstructive sleep apnoea (OSA) have a number of upper airway structural abnormalities which may influence the resistance of the oral airway to airflow. There have been no systematic studies of the flow dynamics of the oral cavity in such patients. METHODS: Inspiratory oral airway resistance to airflow (RO) was measured in 13 awake patients with OSA in both the upright and supine positions (neck position constant). Each subject breathed via a mouthpiece while the nasal airway was occluded with a nasal mask. RESULTS: In the upright position the mean (SE) RO was 1.26 (0. 19) cm H2O/l/s (at 0.4 l/s) which increased to 2.01 (0.43) cm H2O/l/s when supine (p<0.05, paired t test). The magnitude of this change correlated negatively with the respiratory disturbance index (r = -0.60, p = 0.03). CONCLUSION: In awake patients with OSA RO is normal when upright but abnormally raised when in the supine position.

Oral airway flow dynamics in healthy humans.

1. Oral airway resistance (RO) is an important determinant of oro-nasal partitioning of airflow (e.g. during exercise and sleep); however, little is known of factors influencing its magnitude and measurement. 2. We developed a non-invasive standardized technique for measuring RO (based on a modification of posterior rhinomanometry) and examined inspiratory RO in 17 healthy male subjects (age, 36 +/- 2 years (mean +/- s.e.m.); height, 177 +/- 2 cm; weight, 83 +/- 3 kg). 3. Inspiratory RO (at 0.4 l s-1) was 0.86 +/- 0.23 cmH2O l-1 s-1 during resting mouthpiece breathing in the upright posture. RO was unaffected by assumption of the supine posture, tended to decrease with head and neck extension and increased to 1.22 +/- 0.19 cmH2O l-1 s-1 (n = 10 subjects, P < 0.01) with 40-45 deg of head and neck flexion. When breathing via a mouth-mask RO was 2.98 +/- 0.42 cmH2O l-1 s-1 (n = 7) and not significantly different from nasal airway resistance. 4. Thus, in awake healthy male subjects with constant jaw position, RO is unaffected by body posture but increases with modest degrees of head and neck flexion. This influence on upper airway patency may be important when oral route breathing is associated with alterations in head and neck position, e.g. during sleep.

Soft palate muscle responses to negative upper airway pressure.

The afferent pathways and upper airway receptor locations involved in negative upper airway pressure (NUAP) augmentation of soft palate muscle activity have not been defined. We studied the electromyographic (EMG) response to NUAP for the palatinus, tensor veli palatini, and levator veli palatini muscles in 11 adult, supine, tracheostomized, anesthetized dogs. NUAP was applied to the nasal or laryngeal end of the isolated upper airway in six dogs and to four to six serial upper airway sites from the nasal cavity to the subglottis in five dogs. When NUAP was applied at the larynx, peak inspiratory EMG activity for the palatinus and tensor increased significantly (P < 0.05) and plateaued at a NUAP of -10 cmH2O. Laryngeal NUAP failed to increase levator activity consistently. Nasal NUAP did not increase EMG activity for any muscle. Consistent NUAP reflex recruitment of soft palate muscle activity only occurred when the larynx was exposed to the stimulus and, furthermore, was abolished by bilateral section of the internal branches of the superior laryngeal nerves. We conclude that soft palate muscle activity may be selectively modulated by afferent activity originating in the laryngeal and hypopharyngeal airway.

Nasal dilator strips delay the onset of oral route breathing during exercise.

The external nasal dilator strip (ENDS) device (Breathe Right, CNS Inc., Chanhassen, MN, USA) has been adopted by athletes to promote nasal route breathing during exercise. We studied the influence of ENDS on the switching point from nasal-only to oro-nasal breathing during exercise in 4 healthy men (age 25 +/- 2 yrs, mean +/- SEM) and 5 women (age 30 +/- 5 yrs). Resting inspiratory nasal airflow resistance decreased from 0.33 +/- 0.02 kPa/L/s without ENDS to 0.22 +/- 0.01 kPa/L/s with ENDS (p < 0.01). ENDS delayed the onset of oro-nasal breathing such that the time from commencement of exercise to switching increased by 15.2%, and maximum levels of inspiratory nasal airflow and ventilation achieved prior to switching increased by 14.9% and 14.3%, respectively (all p < 0.05). We conclude that, in normal healthy subjects, ENDS does promote nasal route breathing during exercise, but any delay in the onset of oral route breathing during a progressive exercise task appears relatively small.

Epiglottic movements during breathing in humans.

1. Using X-ray fluoroscopy we measured antero-posterior (A-P) and cranio-caudal (C-C) displacements of the epiglottic tip (ET), corniculate cartilage and hyoid bone in seven seated, normal human subjects (age 34 +/- 3 years; mean +/- S.E.M.; 4 males, 3 females) breathing via a nasal mask or mouthpiece with (RL) and without (UB) a fixed resistive load. 2. During UB, via either mouth or nose, there were no significant A-P ET movements. During RL via the nose the ET at peak expiratory flow was 2.6 +/- 1.3 mm cranial to its position at peak inspiratory flow (P < 0.05, ANOVA). C-C movements of the ET correlated strongly with C-C movements of the corniculate cartilage and hyoid bone. 3. The ET, corniculate cartilage and hyoid bone (at zero airflow) were situated more caudally during oral UB than for any other condition. 4. When present, epiglottic movements during breathing do not appear to be independent of those of the larynx and hyoid. Furthermore, epiglottic position may be related to the level of upper airway resistance.

Mechanical properties of the upper airway.

Abnormalities of upper airway mechanical properties are a well-recognized and important feature of the pathophysiology of the obstructive sleep apnea hypopnea syndrome (OSAHS). Recently, investigations enhanced our understanding of the factors that promote upper airway obstruction. In patients with OSAHS, anatomic narrowing of the pharyngeal airway, particularly in the lateral dimension with thickening of the lateral pharyngeal walls, is present. In addition, the passive upper airway (absent muscle activity) demonstrates increased collapsibility, which is modulated by caudal tracheal traction, mucosal surface forces, route of breathing, and the balance of intraluminal airway and extraluminal tissue pressures. In patients with OSAHS, pharyngeal dilator muscles (including the genioglossus and soft palate muscles) demonstrate a coordinated pattern of increased muscle activity while awake compared with normals. This is thought to represent a neuromuscular compensatory mechanism for the anatomically narrow, more collapsible upper airway. With the onset of sleep, the reflexes that drive this muscular compensation are diminished, leading to reduced muscle activity and predisposing the OSAHS patient to pharyngeal collapse. Better understanding of the mechanical properties of the upper airway in normals and patients with OSAHS should help in the development of new therapeutic strategies.

Supraglottic airway pressure-flow relationships during oronasal airflow partitioning in dogs.

We studied pressure-flow relationships in the supraglottic airway of eight prone mouth-open anesthetized (intravenous chloralose or pentobarbital sodium) crossbred dogs (weight 15-26 kg) during increasing respiratory drive (CO2 administration; n = 4) and during graded-voltage electrical stimulation (SV; n = 4) of the soft palate muscles. During increased respiratory drive, inspiratory airflow occurred via both the nose (Vn) and mouth (Vm), with the ratio of Vn to Vm [%(Vn/Vm)] decreasing maximally from 16.0 +/- 7.0 (SD) to 2.4 +/- 1.6% (P < 0.05). Simultaneously, oral airway resistance at peak inspiratory flow decreased from 2.1 +/- 1.0 to 0.4 +/- 0.4 cmH2O (P < 0.05), whereas nasal airway resistance did not change (14.4 +/- 7.2 to 13.1 +/- 5.4 cmH2O; P = 0.29). Inspiratory pressure-flow plots of the oral airway were inversely curvilinear or more complex in nature. Nasal pathway plots, however, demonstrated a positive linear relationship in all animals (r = 0.87 +/- 0.11; all P < 0.001). During electrical stimulation of soft palate muscle contraction accompanied by graded constant-inspiratory airflows of 45-385 ml/s through an isolated upper airway, %(Vn/Vm) decreased from 69 +/- 50 to 10 +/- 13% at a SV of 84 +/- 3% of maximal SV (P < 0.001). At a SV of 85 +/- 1% of maximum, normalized oral airway resistance (expressed as percent baseline) fell to 5 +/- 3%, whereas normalized nasal resistance was 80 +/- 9% (both P < 0.03). Thus control of oronasal airflow partitioning in dogs appears mediated more by alterations in oral route geometry than by closure of the nasopharyngeal airway.

Control of epiglottic position in dogs: role of negative upper airway pressure.

We investigated the influence of negative upper airway pressure (NUAP) on hyoepiglotticus and genioglossus muscle electromyographic (EMG) activity in anaesthetised (sodium pentobarbitone/ chloralose) dogs breathing via a tracheostomy. Changes in pressure were not transmitted through the entire upper airway, thus confirming airway occlusion during NUAP. When NUAP was applied at the larynx, peak inspiratory and tonic EMG activity of the genioglossus and HE both increased significantly (p < 0.05) and reached a plateau at NUAP of -10 to -20 cmH2O. Nasal NUAP at any level failed to influence either genioglossus or HE EMG activity. Following bilateral section of the internal branches of the superior laryngeal nerves (SLNin), resting levels of HE and genioglossus EMG activity decreased to virtually zero. Moreover, NUAP applied at the larynx now failed to recruit EMG activity for either muscle. These findings suggest active control of epiglottic position in dogs during NUAP.