Upper airway muscle and diaphragm responses to hypoxia in the piglet

1990 ◽  
Vol 68 (2) ◽  
pp. 672-677 ◽  
Author(s):  
R. J. Martin ◽  
E. van Lunteren ◽  
M. A. Haxhiu ◽  
W. A. Carlo

The neonatal ventilatory response to hypoxia is characterized by initial transient stimulation and subsequent respiratory depression. It is unknown, however, whether this response is also exhibited by the upper airway muscles that regulate nasal, laryngeal, and pharyngeal patency. We therefore compared electromyogram (EMG) amplitudes and minute EMGs for the diaphragm (DIA), alae nasi (AN), posterior cricoarytenoid (PCA), and genioglossus (GG) muscles in 12 anesthetized spontaneously breathing piglets during inhalation of 12% O2 over 10 min. Minute EMG for the DIA responded to hypoxia with an initial transient increase and subsequent return to prehypoxia levels by 10 min. Hypoxia also stimulated all three upper airway muscles. In contrast to the DIA EMG, however, AN, PCA, and GG EMGs all remained significantly above prehypoxia levels after 10 min of hypoxia. We have thus demonstrated that the initial stimulation and subsequent depression of the DIA EMG after 12% O2 inhalation contrast with the sustained increase in AN, PCA, and GG EMGs during hypoxia. We speculate that 1) central inhibition during neonatal hypoxia is primarily distributed to the motoneuron pools regulating DIA activation and 2) peripheral chemoreceptor stimulation and/or central disinhibition induced by hypoxia preferentially influence those motoneuron pools that regulate upper airway muscle activation, causing the different hypoxic responses of these muscle groups in the young piglet.

1990 ◽  
Vol 68 (3) ◽  
pp. 1041-1047 ◽  
Author(s):  
W. A. Carlo ◽  
J. M. DiFiore

Upper airway muscles and the diaphragm may have different quantitative responses to chemoreceptor stimulation. To compare the respiratory muscle responses to changes in CO2, 10 ventilator-dependent preterm infants (gestational age 28 +/- 1 wk, postnatal age 40 +/- 6 days, weight 1.4 +/- 0.1 kg) were passively hyperventilated to apnea and subsequently hypoventilated. Electromyograms from the genioglossus, alae nasi, posterior cricoarytenoid, and diaphragm were recorded from surface electrodes. Apneic CO2 thresholds of all upper airway muscles (genioglossus 46.8 +/- 4.3 Torr, alae nasi 42.4 +/- 3.6 Torr, posterior cricoarytenoid 41.6 +/- 3.2 Torr) were higher than those of the diaphragm (38.8 +/- 2.6 Torr, all P less than 0.05). Above their CO2 threshold levels, responses of all upper airway muscles appeared proportional to those of the diaphragm. We conclude that nonproportional responses of the respiratory muscles to hypercapnia may be the result of differences in their CO2 threshold. These differences in CO2 threshold may cause imbalance in respiratory muscle activation with changes in chemical drive, leading to upper airway instability and obstructive apnea.


1983 ◽  
Vol 55 (6) ◽  
pp. 1837-1843 ◽  
Author(s):  
M. A. Haxhiu ◽  
E. C. Deal ◽  
W. B. Van de Graaff ◽  
E. Van Lunteren ◽  
J. A. Salamone ◽  
...  

The effect of bronchoconstriction on the activity of the diaphragm and the upper dilating airway muscles were studied by administering graded doses of methacholine to anesthetized dogs spontaneously breathing oxygen. The electrical activity of the genioglossus, posterior cricoarytenoid, and alae nasi was compared with that of the diaphragm at different levels of pulmonary resistance. Induced bronchoconstriction was associated with increases in the electrical activity of all muscles examined. Bilateral cervical vagotomy diminished but did not prevent the bronchoconstrictor effects of methacholine. When greater concentrations of methacholine were administered to produce bronchoconstriction comparable with that produced prevagotomy, both genioglossus and diaphragm activity increased. This study indicates that the upper airway muscles and the diaphragm respond to bronchoconstriction. The activation of the upper airway muscles with bronchoconstriction may decrease upper airway resistance serving to partially offset increases in pulmonary resistance and to modulate airflow patterns during bronchoconstriction.


1984 ◽  
Vol 56 (3) ◽  
pp. 730-736 ◽  
Author(s):  
E. van Lunteren ◽  
K. P. Strohl ◽  
D. M. Parker ◽  
E. N. Bruce ◽  
W. B. Van de Graaff ◽  
...  

The effects of vagally mediated volume-related feedback on the activity of upper airway muscles was assessed in nine pentobarbital-anesthetized, tracheostomized, spontaneously breathing dogs. Moving average electrical activity was recorded before and during single-breath airway occlusions from the genioglossus, posterior cricoarytenoid, and alae nasi muscles and compared with simultaneously recorded tidal volume and electrical activity of the phrenic nerve (6 dogs) or diaphragm (3 dogs). The normally early peak of upper airway muscle activity during unoccluded breaths was delayed to late or end inspiration during occluded breaths. Inspiratory depression started at a lower volume above end-expiratory volume and at an earlier time after inspiratory onset for the upper airway muscles than for the phrenic nerve and the diaphragm. The amount of depression at the end of inspiratory airflow was larger for all of the upper airway muscles than for the phrenic nerve and diaphragm. Depressive effects were most prominent in the genioglossus, followed by the posterior cricoarytenoid and the alae nasi. After vagotomy, depressive effects of volume-related feedback were no longer seen. These results suggest that activity of the upper airway muscles is modulated by vagally mediated feedback, apparently to a larger extent than that of the diaphragm and phrenic nerve.


1986 ◽  
Vol 61 (6) ◽  
pp. 2122-2128 ◽  
Author(s):  
D. E. Weese-Mayer ◽  
R. T. Brouillette ◽  
L. M. Klemka ◽  
C. E. Hunt

We previously demonstrated dose-dependent increases in both hypoglossal and phrenic electroneurograms after almitrine in anesthetized, paralyzed, and vagotomized cats. We have now investigated the effect of this peripheral chemoreceptor stimulant on diaphragmatic and genioglossal (GG, an upper airway-maintaining muscle) electromyograms in five unanesthetized, chronically instrumented, spontaneously breathing adult cats during slow-wave sleep. In 12 studies almitrine doses of 1.0–6.0 mg/kg increased inspired minute ventilation (VI), frequency (f), and tidal volume (VT) and decreased expiratory time (TE). However, almitrine doses as high as 6.0 mg/kg failed to augment phasic inspiratory GG activity. To determine why almitrine induced phasic inspiratory upper airway activity in anesthetized, vagotomized cats but not in sleeping cats, additional studies were performed. In four dose-response studies in three pentobarbital-anesthetized cats, almitrine, 1.0–6.0 mg/kg, did not produce phasic inspiratory GG activity. Almitrine did induce phasic inspiratory GG activity in two of three studies in three vagotomized, tracheostomized, alpha-chloralose-urethan-anesthetized cats. These results suggest that almitrine would not be useful in obstructive sleep apnea, yet because almitrine markedly increased VI, f, and VT and decreased TE in unanesthetized sleeping cats the drug may be effective in patients who lack normal central neural respiratory drive, such as the preterm infant.


1984 ◽  
Vol 56 (3) ◽  
pp. 746-752 ◽  
Author(s):  
E. van Lunteren ◽  
W. B. Van de Graaff ◽  
D. M. Parker ◽  
J. Mitra ◽  
M. A. Haxhiu ◽  
...  

The effects of negative pressure applied to just the upper airway on nasal and laryngeal muscle activity were studied in 14 spontaneously breathing anesthetized dogs. Moving average electromyograms were recorded from the alae nasi (AN) and posterior cricoarytenoid (PCA) muscles and compared with those of the genioglossus (GG) and diaphragm. The duration of inspiration and the length of inspiratory activity of all upper airway muscles was increased in a graded manner proportional to the amount of negative pressure applied. Phasic activation of upper airway muscles preceded inspiratory activity of the diaphragm under control conditions; upper airway negative pressure increased this amount of preactivation. Peak diaphragm activity was unchanged with negative pressure, although the rate of rise of muscle activity decreased. The average increases in peak upper airway muscle activity in response to all levels of negative pressure were 18 +/- 4% for the AN, 27 +/- 7% for the PCA, and 122 +/- 31% for the GG (P less than 0.001). Rates of rise of AN and PCA electrical activity increased at higher levels of negative pressure. Nasal negative pressure affected the AN more than the PCA, while laryngeal negative pressure had the opposite effect. The effects of nasal negative pressure could be abolished by topical anesthesia of the nasal passages, while the effects of laryngeal negative pressure could be abolished by either topical anesthesia of the larynx or section of the superior laryngeal nerve. Electrical stimulation of the superior laryngeal nerve caused depression of AN and PCA activity, and hence does not reproduce the effects of negative pressure.(ABSTRACT TRUNCATED AT 250 WORDS)


PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253060
Author(s):  
M. Nicholas Musselwhite ◽  
Tabitha Y. Shen ◽  
Melanie J. Rose ◽  
Kimberly E. Iceman ◽  
Ivan Poliacek ◽  
...  

The role of the cerebellum in controlling the cough motor pattern is not well understood. We hypothesized that cerebellectomy would disinhibit motor drive to respiratory muscles during cough. Cough was induced by mechanical stimulation of the tracheobronchial airways in anesthetized, spontaneously breathing adult cats (8 male, 1 female), and electromyograms (EMGs) were recorded from upper airway, chest wall, and abdominal respiratory muscles. Cough trials were performed before and at two time points after total cerebellectomy (10 minutes and >1 hour). Unlike a prior report in paralyzed, decerebrated, and artificially ventilated animals, we observed that cerebellectomy had no effect on cough frequency. After cerebellectomy, thoracic inspiratory muscle EMG magnitudes increased during cough (diaphragm EMG increased by 14% at 10 minutes, p = 0.04; parasternal by 34% at 10 minutes and by 32% at >1 hour, p = 0.001 and 0.03 respectively). During cough at 10 minutes after cerebellectomy, inspiratory esophageal pressure was increased by 44% (p = 0.004), thyroarytenoid (laryngeal adductor) muscle EMG amplitude increased 13% (p = 0.04), and no change was observed in the posterior cricoarytenoid (laryngeal abductor) EMG. Cough phase durations did not change. Blood pressure and heart rate were reduced after cerebellectomy, and respiratory rate also decreased due to an increase in duration of the expiratory phase of breathing. Changes in cough-related EMG magnitudes of respiratory muscles suggest that the cerebellum exerts inhibitory control of cough motor drive, but not cough number or phase timing in response to mechanical stimuli in this model early after cerebellectomy. However, results varied widely at >1 hour after cerebellectomy, with some animals exhibiting enhancement or suppression of one or more components of the cough motor behavior. These results suggest that, while the cerebellum and behavior-related sensory feedback regulate cough, it may be difficult to predict the nature of the modulation based on total cerebellectomy.


1980 ◽  
Vol 49 (4) ◽  
pp. 638-642 ◽  
Author(s):  
K. P. Strohl ◽  
M. J. Hensley ◽  
M. Hallett ◽  
N. A. Saunders ◽  
R. H. Ingram

Animal studies have shown activation of upper airway muscles prior to inspiratory efforts of the diaphragm. To investigate this sequence of activation in humans, we measured the electromyogram (EMG) of the alae nasi (AN) and compared the time of onset of EMG to the onset of inspiratory airflow, during wakefulness, stage II or III sleep (3 subj), and CO2-induced hyperpnea (6 subj). During wakefulness, the interval between AN EMG and airflow was 92 +/- 34 ms (mean +/- SE). At a CO2 level of greater than or equal to 43 Torr, the AN EMG to airflow was 316 +/- 38 ms (P < 0.001). During CO2-induced hyperpnea, the AN EMG to airflow interval and AN EMG magnitude increased in direct proportion to CO2 levels and minute ventilation. During stages II and III of sleep, the interval between AN EMG and airflow increased when compared to wakefulness (P < 0.005). We conclude that a sequence of inspiratory muscle activation is present in humans and is more apparent during sleep and during CO2-induced hyperpnea than during wakefulness.


2006 ◽  
Vol 101 (5) ◽  
pp. 1377-1385 ◽  
Author(s):  
E. Fiona Bailey ◽  
Yu-Hsien Huang ◽  
Ralph F. Fregosi

We recently showed respiratory-related coactivation of both extrinsic and intrinsic tongue muscles in the rat. Here, we test the hypothesis that intrinsic tongue muscles contribute importantly to changes in velopharyngeal airway volume. Spontaneously breathing anesthetized rats were placed in a MRI scanner. A catheter was placed in the hypopharynx and connected to a pressure source. Axial and sagittal images of the velopharyngeal airway were obtained, and the volume of each image was computed at airway pressures ranging from +5.0 to −5.0 cmH2O. We obtained images in the hypoglossal intact animal (i.e., coactivation of intrinsic and extrinsic tongue muscles) and after selective denervation of the intrinsic tongue muscles, with and without electrical stimulation. Denervation of the intrinsic tongue muscles reduced velopharyngeal airway volume at atmospheric and positive airway pressures. Electrical stimulation of the intact hypoglossal nerve increased velopharyngeal airway volume; however, when stimulation was repeated after selective denervation of the intrinsic tongue muscles, the increase in velopharyngeal airway volume was significantly attenuated. These findings support our working hypothesis that intrinsic tongue muscles play a critical role in modulating upper airway patency.


1984 ◽  
Vol 56 (3) ◽  
pp. 737-745 ◽  
Author(s):  
E. van Lunteren ◽  
M. A. Haxhiu ◽  
J. Mitra ◽  
N. S. Cherniack

Recent studies have suggested that the upper airway muscles receive a substantial portion of their excitatory input from the peripheral chemoreceptors. We examined the responses of the phrenic, hypoglossal, and recurrent laryngeal nerves to agents that are known to modify carotid body activity. Dopamine, an inhibitor, and isoproterenol and lobeline, two stimulators of carotid body activity, were administered into the lingual arteries of 14 anesthetized, paralyzed cats artificially ventilated with 100% O2. Dopamine decreased the activity of all three nerves (P less than 0.001) but inhibited the hypoglossal nerve more than the phrenic and recurrent laryngeal nerves (P less than 0.001). Isoproterenol and lobeline increased the activity of all three nerves (P less than 0.001) but stimulated the hypoglossal nerve more than the phrenic and recurrent laryngeal nerves (P less than 0.001). These relatively greater effects of all three agents on the hypoglossal nerve compared with the phrenic and the recurrent laryngeal nerves persisted under both hypoxic and hypercapnic conditions. After midcervical vagotomy, the responses of the hypoglossal to all three drugs remained larger than those of the phrenic nerve. After combined vagotomy and carotid sinus nerve section, the stimulatory effects of lobeline and the inhibitory effects of dopamine were no longer apparent. We conclude that it is possible to preferentially alter respiratory-related activity of the hypoglossal nerve compared with that of the phrenic nerve using agents that modify peripheral chemoreceptor activity.


2001 ◽  
Vol 91 (2) ◽  
pp. 897-904 ◽  
Author(s):  
M. H. Stella ◽  
S. J. England

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.


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