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Biomedical subjects

T C Amis

Publications and source records attributed to T C Amis.

At least 19 recordsLinked to original sources

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.

Adult

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.

Adolescent

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.

Airway Resistance

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.

Animals

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.

Adult

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.

Adult

Electromyographic activity of the hyoepiglotticus muscle in dogs.

We examined the respiratory-related electromyographic (EMG) activity of the hyoepiglotticus muscle using fine wire bipolar electrodes, inserted perorally in five anaesthetised (IV chloralose) tracheostomised dogs studied in the prone, mouth open position. The integrated HE EMG was measured in arbitrary units (a.u.) during resting breathing via the upper airway, and on a breath-by-breath basis during progressive increases in respiratory drive induced by infusion of CO2 into the inspired gas. The HE demonstrated inspiratory activity which increased linearly in relation to ventilation (r = 0.85 +/- 0.06, p < 0.001) due to an increase in both phasic (8.8 +/- 1.8 to 32.4 +/- 9.2 a.u.) and tonic (0.2 +/- 0.1 to 26.3 +/- 13.3 a.u.) activity (both p < 0.05). In addition, HE EMG developed substantial phasic expiratory activity (1.3 +/- 1.1 to 13.8 +/- 4.4 a.u., p < 0.05). We conclude that the canine HE exhibits inspiratory and expiratory related activity which is augmented during increased respiratory drive. These findings imply active control of epiglottic position during breathing in dogs.

Animals

Mechanisms of oronasal airflow partitioning in dogs.

We examined the integrated (MTA) electromyographic activity (EMG) of the hyoepiglotticus (HE) muscle and the soft palate muscles (SPM) during CO2 administration in 6 anaesthetised prone, mouth open dogs. As ventilation increased nasal flow (VN) as a percentage of total flow (VT), i.e. VN/VT%, decreased. Breath-by-breath peak inspiratory and peak expiratory HE EMG activity was strongly and inversely correlated with VN/VT% (both r > 0.8, p < 0.001), whereas the correlation between SPM MTA EMG activity and VN/VT% was highly variable. Severing of the HE muscles halved the rate at which VN/VT% was reduced with respect to increasing ventilation while electrical stimulation of HE muscle contraction resulted in a fall in VN/VT% to near zero levels. Active control of epiglottic position appears to be an important mechanism controlling the patency of the epiglottic-soft palate seal and thus the oronasal partitioning of airflow in dogs.

Anesthesia, General

Influence of hyoepiglotticus muscle contraction on canine upper airway geometry.

We examined the effect of hyoepiglotticus (HE) muscle contraction on epiglottic position in 4 anaesthetised (IV choralose, pentobarbitone sodium) tracheostomised, mechanically ventilated dogs studied in the prone mouth open position. Computerised axial tomography (coronal plane) was used to measure the vertical distance between the tip of the epiglottis (E) and (1) the soft palate (SP) (i.e. E-SP distance) and (2) the dorsal wall of the nasopharynx (N) (i.e. E-N distance). Duplicate runs of graded electrical stimulation of the HE muscle, using bilateral bipolar fine wire electrodes, were performed in each animal and resulted in a progressive increase in both the E-SP distance (baseline of 0.5 +/- 0.5 to a maximum of 13.1 +/- 2.3 mm, mean +/- SE) and the E-N distance (29.1 +/- 2.0 to a maximum of 42.2 +/- 2.7 mm, both p < 0.02). We conclude that HE contraction moves the epiglottis ventrally away from the soft palate thus opening and enlarging the oral pathway for airflow.

Animals

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.

Airway Obstruction

Influence of upper airway pressure oscillations on soft palate muscle electromyographic activity.

Snoring is characterized by high-frequency (30-50 Hz) pressure oscillations (HFPO) in the upper airway (UA). The soft palate is a major oscillating structure during snoring, and soft palate muscle (SPM) activity is an important determinant of velopharyngeal patency. Consequently, we examined the effect of artificial HFPO applied to the UA on the integrated electromyographic (EMG) activity of the SPMs in 11 supine mouth-closed anesthetized (pentobarbital sodium/chloralose) dogs breathing spontaneously via a tracheostomy. The EMGs of the palatinus (Pal; n = 11), levator veli palatini (LP; n = 9), and tensor veli palatini (TP; n = 8) were monitored with intramuscular fine-wire electrodes. Peak inspiratory and peak expiratory EMG activity was measured in arbitrary units (au) as the mean of five consecutive breaths. HFPO [+/- 4.5 +/- 0.4 (SE) cmH2O; 30 Hz] applied at the laryngeal end of the isolated UA increased peak inspiratory EMG from 3.3 +/- 2.0 to 8.4 +/- 1.7 au (P < 0.05) for Pal and from 2.0 +/- 1.1 to 7.3 +/- 2.7 au (P < 0.05) for LP. For the TP, increases were evident in four dogs, but mean values for the group did not change (5.8 +/- 2.4 to 11.0 +/- 4.1 au, P = 0.5). The peak expiratory EMG did not change for any SPM (all P > 0.3). Thus HFPO applied to the UA augments inspiratory SPM activity. Reflex augmentation of SPM activity by HFPO may serve to dilate the retropalatal airway and/or stiffen the soft palate during inspiration in an attempt to stabilize UA geometry during snoring.

Animals

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.

Air Pressure

Thyroid cartilage movements during breathing.

We measured lateral (outward) thyroid cartilage displacement (TCD) of the larynx in six supine anesthetized (intravenous chloralose) dogs. Combined left and right TCDs were measured with linear transducers attached by a thread to the thyroid alae. During tidal breathing via a tracheostomy, phasic inspiratory TCD occurred in all dogs [0.66 +/- 0.2 mm (mean +/- SE)] together with phasic inspiratory electromyographic activity in the cricothyroid (CT) and posterior cricoarytenoid (PCA) muscles. During brief tracheal occlusions, TCD increased significantly to 1.27 +/- 0.2 mm (P = 0.001), accompanied by an increase of 95-115% in the peak CT and PCA electromyograms. Bilateral supramaximal electrical stimulation of the external branches of the superior laryngeal nerve (ExSLN) produced a TCD of 9.9 +/- 0.8 mm; however, similar stimulation of the recurrent laryngeal nerve (RLN) produced a TCD of only 1.33 +/- 0.1 mm (P = 0.0001). Furthermore, bilateral section of the ExSLN in five dogs significantly reduced tidal TCD by 48.7 +/- 24.4% (P < 0.05), and bilateral section of both the ExSLN and RLN resulted in slight phasic inward TCD (-0.06 +/- 0.05 mm). Thus, it appears that the activities of both the CT and RLN-innervated muscles (probably the PCA muscle) contribute to tidal breathing TCD. These findings suggest that inspiratory dilation of the hypopharynx is mediated by contractions of CT and PCA muscles.

Anesthesia

Cardiorespiratory consequences of expiratory chest wall compression during mechanical ventilation and severe hyperinflation.

OBJECTIVES: To measure and compare the effects of manual expiratory compression of either the rib cage or abdomen on cardiac output, end-expiratory lung volume, and other cardiorespiratory variables in an animal model that mimics the severe pulmonary hyperinflation and hemodynamic impairment occurring in patients with severe acute asthma during mechanical ventilation. DESIGN: Prospective, randomized, crossover trial. SETTING: Research laboratory. SUBJECTS: Seven cross-bred, anesthetized, supine dogs. INTERVENTIONS: The following sequence was employed: a) spontaneous breathing without pulmonary hyperinflation; b) positive-pressure ventilation with severe pulmonary hyperinflation (produced by an external variable expiratory flow resistor); c) approximately 7 mins of manual expiratory compression of either the rib cage or abdomen during positive-pressure ventilation-hyperinflation. This sequence was then repeated, incorporating the alternative type of expiratory compression. MEASUREMENTS AND MAIN RESULTS: Cardiac output (measured by thermodilution), aortic pressure, pleural (esophageal) pressure, and changes in end-expiratory lung volume were measured. The decrease in cardiac output due to mechanical ventilation with pulmonary hyperinflation was exacerbated by rib cage compression (p < .001; spontaneous breathing 2.9 +/- 0.2 L/min, hyperinflation 1.5 +/- 0.1 L/min, and rib cage compression 1.0 +/- 0.1 [SEM] L/min). However, the positive-pressure ventilation-hyperinflation-induced decrease in cardiac output was attenuated by abdominal compression (p < .001; spontaneous breathing 3.3 +/- 0.2 L/min, hyperinflation 1.4 +/- 0.1 L/min, and abdominal compression 2.1 +/- 0.1 L/min). Mean aortic pressure returned to prehyperinflation levels during abdominal compression (p < .001; spontaneous breathing 126 +/- 2 mm Hg, hyperinflation 75 +/- 5 mm Hg, and abdominal compression 120 +/- 3 mm Hg). Both types of compression were similarly effective (p > .75) in increasing mean expiratory pleural pressure, so that end-expiratory lung volume was similarly (p > .25) reduced (0.45 +/- 0.05 and 0.40 +/- 0.05 L for rib cage and abdominal compressions, respectively) in this non-air flow, limiting animal model. CONCLUSIONS: The cardiorespiratory effects of manually compressing the rib cage or abdomen during expiration in this animal study suggest that these techniques should be carefully evaluated in mechanically ventilated patients with severe acute asthma.

Abdomen

Measurement of pulmonary diffusing capacity for carbon monoxide and functional residual capacity during rebreathing in conscious thoroughbreds.

A rebreathing method for measurement of pulmonary diffusing capacity for carbon monoxide (DLCO) and functional residual capacity (FRC) was evaluated in conscious horses. Horses were manually ventilated through an endotracheal tube, using a custom-made syringe filled with a gas mixture containing 18-carbon monoxide (18CO) and helium (He). The 18CO and He concentrations were continuously monitored by use of a mass spectrometer connected to the rebreathing circuit. Values for DLCO and FRC were calculated from changes in the concentration of these 2 gases. In 11 Thoroughbreds, mean (+/- SD) DLCO was 330.3 +/- 56.9 ml.min-1 x mm of Hg-1, and FRC was 20.21 +/- 3.35 L. Body weight normalization yielded mean (+/- SD) values of 0.652 +/- 0.114 ml.min-1 x mm of Hg-1 x kg-1 for DLCO, and 39.9 +/- 6.4 ml.kg-1 for FRC.

Animals

Chronic tracheobronchial disease in the dog.

Tracheobronchial collapse and chronic bronchitis (CB) are the two most common forms of chronic tracheobronchial disease in dogs. These conditions may exist independently of one another, although CB and some degree of tracheobronchial collapse often co-exist in the same patient. Diagnosis of CB can be established on clinical grounds alone, whereas radiographic or bronchoscopic evidence is required to confirm the diagnosis of tracheobronchial collapse. Although glucocorticoid drug therapy remains one of the most effective methods for managing CB, surgical implantation of a prosthetic airway device may be of great benefit for some dogs with a focal area of collapsing trachea. With early diagnosis and aggressive medical and surgical management, the prognosis for many dogs with chronic tracheobronchial disease is good for reasonable quality of life.

Animals

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.

Airway Resistance

Pharyngeal dilation associated with cricothyroid muscle contraction in dogs.

The mechanical function of phasic respiratory-related activity of the cricothyroid muscle of the larynx is poorly understood. We studied five adult cross-bred dogs (weight 14-20 kg) deeply anesthetized with pentobarbitone sodium, mechanically ventilated via a tracheostomy, and placed prone with the mouth open. Bilateral cricothyroid muscle contraction was induced by supramaximal electrical stimulation of the external branches of the superior laryngeal nerve. Computerized axial tomography was used to assess effects of cricothyroid muscle contraction. During cricothyroid muscle contraction, oropharyngeal (tip of epiglottis) cross-sectional area increased by 18.0 +/- 3.0% (SE) (P = 0.008), whereas combined left and right piriform recess cross-sectional area increased by 85 +/- 25% (n = 4; P = 0.02) at the midepiglottic level and by 152 +/- 37% (P = 0.01) at the base of the epiglottis. Furthermore, at the base of the epiglottis the maximum horizontal distance between the alae of the thyroid cartilage increased by 21 +/- 8% (P = 0.05). In contrast, lateral glottic diameter decreased by 52 +/- 2% (n = 4; P = 0.01), whereas dorsoventral glottic diameter increased by 18 +/- 5% (n = 4; P less than 0.02). The cricothyroid muscle, therefore, has the capacity to act simultaneously as a pharyngeal dilator and a glottic constrictor and thus may play a role in the control of oropharyngeal as well as laryngeal patency.

Animals