Phasic volume-related feedback on upper airway muscle activity

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.

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)


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.


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.


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.


2001 ◽  
Vol 91 (2) ◽  
pp. 905-911 ◽  
Author(s):  
M. H. Stella ◽  
S. J. England

The hypothesis that respiratory modulation due to upper airway (UA) pressure and flow is dependent on stimulus modality and respiratory phase-specific activation was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. Negative pressure and flow applied to the isolated UA at room or body temperature during inspiration only enhanced posterior cricoarytenoid muscle activity from that present without UA pressure and flow (baseline) by 15–20%. Time shifting the onset of UA flow relative to tracheal flow decreased this enhancement. The same enhancement was observed with oscillatory or constant airflow. UA positive pressure and flow at room or body temperature applied during expiration only enhanced thyroarytenoid muscle activity from baseline by 50–160%. The same enhancement was observed with oscillatory or constant airflow at body temperature. Constant positive pressure and flow enhanced thyroarytenoid muscle activity more than oscillatory pressure and flow at room temperature. We conclude that the respiratory modulation of UA afferents is processed in a phase-specific fashion and is dependent on stimulus modality (tonic vs. phasic).


1997 ◽  
Vol 106 (11) ◽  
pp. 897-901 ◽  
Author(s):  
Robert G. Berkowitz ◽  
John Chalmers ◽  
Qi-Jian Sun ◽  
Paul M. Pilowsky

An anatomic and electrophysiological study of the rat posterior cricoarytenoid (PCA) muscle is described. The intramuscular nerve distribution of the PCA branch of the recurrent laryngeal nerve was demonstrated by a modified Sihler's stain. The nerve to the PCA was found to terminate in superior and inferior branches with a distribution that appeared to be confined to the PCA muscle. Electromyography (EMG) recordings of PCA muscle activity in anesthetized rats were obtained under stereotaxic control together with measurement of phrenic nerve discharge. A total of 151 recordings were made in 7 PCA muscles from 4 rats. Phasic inspiratory activity with a waveform similar to that of phrenic nerve discharge was found in 134 recordings, while a biphasic pattern with both inspiratory and post-inspiratory peaks was recorded from random sites within the PCA muscle on 17 occasions. The PCA EMG activity commenced 24.6 ± 2.2 milliseconds (p < .0001) before phrenic nerve discharge. The results are in accord with findings of earlier studies that show that PCA muscle activity commences prior to inspiratory airflow and diaphragmatic muscle activity. The data suggest that PCA and diaphragm motoneurons share common or similar medullary pre-motoneurons. The earlier onset of PCA muscle activity may indicate a role for medullary pre-inspiratory neurons in initiating PCA activity.


1986 ◽  
Vol 61 (2) ◽  
pp. 719-727 ◽  
Author(s):  
E. van Lunteren ◽  
N. S. Cherniack

In nine anesthetized supine spontaneously breathing dogs, we compared moving average electromyograms (EMGs) of the costal diaphragm and the third parasternal intercostal muscles with their respective respiratory changes in length (measured by sonomicrometry). During resting O2 breathing the pattern of diaphragm and intercostal muscle inspiratory shortening paralleled the gradually incrementing pattern of their moving average EMGs. Progressive hypercapnia caused progressive increases in the amount and velocity of respiratory muscle inspiratory shortening. For both muscles there were linear relationships during the course of CO2 rebreathing between their peak moving average EMGs and total inspiratory shortening and between tidal volume and total inspiratory shortening. During single-breath airway occlusions, the electrical activity of both the diaphragm and intercostal muscles increased, but there were decreases in their tidal shortening. The extent of muscle shortening during occluded breaths was increased by hypercapnia, so that both muscles shortened more during occluded breaths under hypercapnic conditions (PCO2 up to 90 Torr) than during unoccluded breaths under normocapnic conditions. These results suggest that for the costal diaphragm and parasternal intercostal muscles there is a close relationship between their electrical and mechanical behavior during CO2 rebreathing, this relationship is substantially altered by occluding the airway for a single breath, and thoracic respiratory muscles do not contract quasi-isometrically during occluded breaths.


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.


1988 ◽  
Vol 65 (5) ◽  
pp. 2124-2131 ◽  
Author(s):  
W. B. Van de Graaff

Patency of the upper airway (UA) is usually considered to be maintained by the activity of muscles in the head and neck. These include cervical muscles that provide caudal traction on the UA. The thorax also applies caudal traction to the UA. To observe whether this thoracic traction can also improve UA patency, we measured resistance of the UA (RUA) during breathing in the presence and absence of UA muscle activity. Fifteen anesthetized dogs breathed through tracheostomy tubes. RUA was calculated from the pressure drop of a constant flow through the isolated UA. RUA decreased 31 +/- 5% (SEM) during inspiration. After hyperventilating seven of these dogs to apnea, we maximally stimulated the phrenic nerves to produce paced diaphragmatic breathing. Despite absence of UA muscle activity, RUA fell 51 +/- 11% during inspiration. Graded changes were produced by reduced stimulation. In six other dogs we denervated all UA muscles. RUA still fell 25 +/- 7% with inspiration in these spontaneously breathing animals. When all caudal ventrolateral cervical structures mechanically linking the thorax to the UA were severed, RUA increased and respiratory fluctuations ceased. These findings indicate that tonic and phasic forces generated by the thorax can improve UA patency. Inspiratory increases in UA patency cannot be attributed solely to activity of UA muscles.


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.


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