Mechano- and chemoreceptor modulation of respiratory muscles in response to upper airway negative pressure

1994 ◽  
Vol 76 (6) ◽  
pp. 2656-2662 ◽  
Author(s):  
E. B. Gauda ◽  
T. P. Carroll ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
R. S. Fitzgerald
Keyword(s):  
Negative Pressure ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Reflex Response ◽  
Emg Activity ◽  
Tracheal Occlusion ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Reflex Activation ◽  
Spontaneously Breathing

To investigate the influence of phasic pulmonary stretch receptors (n = 6) and chemoreceptors (n = 7) on the reflex response of the genioglossus (GG) muscle and diaphragm (DIA) to upper airway (UAW) negative pressure, we measured the response of the GG and DIA electromyogram (EMG) to three challenges: 1) negative pressure applied to the UAW during normoxia and hypercapnia, 2) end-expiratory tracheal occlusion, and 3) application of UAW negative pressure simultaneous with tracheal occlusion in spontaneously breathing tracheotomized anesthetized cats. Peak GG EMG was greatest when UAW negative pressure and end-expiratory tracheal occlusion were combined. No GG EMG activity was seen when UAW negative pressure was applied alone unless the animal was vagotomized or hypercapnic. DIA EMG increased in response to UAW negative pressure combined with occlusion. However, the increase in peak GG EMG was significantly greater than for the DIA with the same challenge. DIA EMG amplitude increased in response to occlusion alone but did not change when UAW negative pressure was applied alone. In the cat, phasic feedback from phasic pulmonary stretch receptors is a potent inhibitor of reflex activation of the GG in response to negative pressure applied to the UAW, which can be overridden by an increase in chemoreceptor drive.

scholarly journals Modulation of laryngeal and respiratory pump muscle activities with upper airway pressure and flow

2001 ◽  
Vol 91 (2) ◽  
pp. 897-904 ◽  
Author(s):  
M. H. Stella ◽  
S. J. England
Keyword(s):  
Negative Pressure ◽  
Muscle Activity ◽  
Upper Airway ◽  
Abdominal Muscle ◽  
Positive Pressure ◽  
Emg Activity ◽  
Posterior Cricoarytenoid ◽  
Spontaneously Breathing ◽  
Respiratory Muscle Activity ◽  
Stimulation Of

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.

scholarly journals Effect of upper airway negative pressure on inspiratory drive during sleep

1998 ◽  
Vol 84 (3) ◽  
pp. 1063-1075 ◽  
Author(s):  
P. R. Eastwood ◽  
A. K. Curran ◽  
C. A. Smith ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Negative Pressure ◽  
Upper Airway ◽  
Resistive Load ◽  
Rapid Eye Movement ◽  
Inhibitory Effects ◽  
Lung Inflation ◽  
Tracheal Occlusion ◽  
Tracheal Pressure

To determine the effect of upper airway (UA) negative pressure and collapse during inspiration on regulation of breathing, we studied four unanesthetized female dogs during wakefulness and sleep while they breathed via a fenestrated tracheostomy tube, which was sealed around the permanent tracheal stoma. The snout was sealed with an airtight mask, thereby isolating the UA when the fenestration (Fen) was closed and exposing the UA to intrathoracic pressure changes, but not to flow changes, when Fen was open. During tracheal occlusion with Fen closed, inspiratory time (Ti) increased during wakefulness, non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep (155 ± 8, 164 ± 11, and 161 ± 32%, respectively), reflecting the removal of inhibitory lung inflation reflexes. During tracheal occlusion with Fen open (vs. Fen closed): 1) the UA remained patent; 2) Ti further increased during wakefulness and NREM (215 ± 52 and 197 ± 28%, respectively) but nonsignificantly during REM sleep (196 ± 42%); 3) mean rate of rise of diaphragm EMG (EMGdi/Ti) and rate of fall of tracheal pressure (Ptr/Ti) were decreased, reflecting an additional inhibitory input from UA receptors; and 4) both EMGdi/Ti and Ptr/Ti were decreased proportionately more as inspiration proceeded, suggesting greater reflex inhibition later in the effort. Similar inhibitory effects of exposing the UA to negative pressure (via an open tracheal Fen) were seen when an inspiratory resistive load was applied over several breaths during wakefulness and sleep. These inhibitory effects persisted even in the face of rising chemical stimuli. This inhibition of inspiratory motor output is alinear within an inspiration and reflects the activation of UA pressure-sensitive receptors by UA distortion, with greater distortion possibly occurring later in the effort.

scholarly journals A secondary reflex suppression phase is present in genioglossus but not tensor palatini in response to negative upper airway pressure

2010 ◽  
Vol 108 (6) ◽  
pp. 1619-1624 ◽  
Author(s):  
Danny J. Eckert ◽  
Julian P. Saboisky ◽  
Amy S. Jordan ◽  
David P. White ◽  
Atul Malhotra
Keyword(s):  
Negative Pressure ◽  
Airway Pressure ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Reflex Responses ◽  
Suppression Phase ◽  
Tonic Muscle ◽  
State Dependent ◽  
Pressure Peak ◽  
Inhibitory Components

On the basis of recent reports, the genioglossus (GG) negative-pressure reflex consists initially of excitation followed by a secondary state-dependent suppression phase. The mechanistic origin and functional role of GG suppression is unknown but has been hypothesized to arise from transient inhibition of respiratory active neurons as a protective reflex to prevent aspiration, as observed in other respiratory muscles (e.g., diaphragm) during airway occlusion. Unlike GG, tensor palatini (TP) is a tonic muscle with minimal respiratory phasic activation during relaxed breathing, although both muscles are important in preserving pharyngeal patency. This study aimed to compare GG vs. TP reflex responses to the same negative-pressure stimulus. We hypothesized that reflex suppression would be present in GG, but not TP. Intramuscular GG and TP EMGs were recorded in 12 awake, healthy subjects (6 female). Reflex responses were generated via 250-ms pulses of negative upper airway pressure (approximately −16 cmH2O mask pressure) delivered in early inspiration. GG and TP demonstrated reflex activation in response to negative pressure (peak latency 31 ± 4 vs. 31 ± 6 ms and peak amplitude 318 ± 55 vs. 314 ± 26% baseline, respectively). A secondary suppression phase was present in 8 of 12 subjects for GG (nadir latency 54 ± 7 ms, nadir amplitude 64 ± 6% baseline), but not in any subject for TP. These data provide further support for the presence of excitatory and inhibitory components of GG (phasic muscle) in response to brief upper airway negative-pressure pulses. Conversely, no reflex suppression below baseline was present in TP (tonic muscle) in response to the same stimuli. These differential responses support the hypothesis that GG reflex suppression may be mediated via inhibition of respiratory-related premotor input.

scholarly journals Differential effects of acute cerebellectomy on cough in spontaneously breathing cats

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253060
Author(s):  
M. Nicholas Musselwhite ◽  
Tabitha Y. Shen ◽  
Melanie J. Rose ◽  
Kimberly E. Iceman ◽  
Ivan Poliacek ◽  
...  
Keyword(s):  
Motor Behavior ◽  
Motor Pattern ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Adductor Muscle ◽  
Motor Drive ◽  
Mechanical Stimuli ◽  
Posterior Cricoarytenoid ◽  
Spontaneously Breathing

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.

Interaction between upper airway negative pressure pulses and CO2 on breathing pattern

1988 ◽  
Vol 65 (1) ◽  
pp. 205-209 ◽  
Author(s):  
D. L. Woodall ◽  
O. P. Mathew
Keyword(s):  
Closed System ◽  
Negative Pressure ◽  
Breathing Pattern ◽  
Upper Airway ◽  
System A ◽  
Pressure Pulses ◽  
Inspiratory Activity ◽  
Resultant Increase ◽  
Breathing Room ◽  
Spontaneously Breathing

The interaction between CO2 and negative pressure pulses on breathing pattern was investigated in 10 anesthetized, spontaneously breathing rabbits. The upper airway was functionally isolated into a closed system. A servo-respirator triggered by the inspiratory activity of the diaphragm was used to apply pressure pulses of -15 cmH2O to the isolated upper airway in early inspiration while the animal was breathing room air, 100% O2, 6% CO2 in O2, or 9% CO2 in O2. The negative pressure pulses produced a reversible inhibition of inspiration in most trials with resultant increase in inspiratory duration (TI); no change was observed in peak diaphragmatic electromyogram (Dia EMG) or expiratory duration, whereas a decrease was seen in mean inspiratory drive (peak Dia EMG/TI). This prolongation of inspiratory duration and decrease in mean inspiratory drive with negative pressure pulses persisted at higher levels of CO2; the slopes of the test breaths were not significantly different from that of control breaths. These results suggest that upper airway negative pressure pulses are equally effective in altering the breathing pattern at all levels of CO2.

Modulation of upper airway muscle activities by bronchopulmonary afferents

2006 ◽  
Vol 101 (2) ◽  
pp. 609-617 ◽  
Author(s):  
E. Fiona Bailey ◽  
Ralph F. Fregosi
Keyword(s):  
Airway Obstruction ◽  
Upper Airway ◽  
Review Of The Literature ◽  
Lung Inflation ◽  
Hyoid Arch ◽  
Lack Of Information ◽  
Stretch Receptors ◽  
C Fiber ◽  
Pulmonary Stretch Receptors ◽  
Upper Airway Muscles

Here we review the influence of bronchopulmonary receptors (slowly and rapidly adapting pulmonary stretch receptors, and pulmonary/bronchial C-fiber receptors) on respiratory-related motor output to upper airway muscles acting on the larynx, tongue, and hyoid arch. Review of the literature shows that all muscles in all three regions are profoundly inhibited by lung inflation, which excites slowly adapting pulmonary stretch receptors. This widespread coactivation includes the recruitment of muscles that have opposing mechanical actions, suggesting that the stiffness of upper airway muscles is highly regulated. A profound lack of information on the modulation of upper airway muscles by rapidly adapting receptors and bronchopulmonary C-fiber receptors prohibits formulation of a conclusive opinion as to their actions and underscores an urgent need for new studies in this area. The preponderance of the data support the view that discharge arising in slowly adapting pulmonary stretch receptors plays an important role in the initiation of the widespread and highly coordinated recruitment of laryngeal, tongue, and hyoid muscles during airway obstruction.

Differential response of respiratory muscles to airway occlusion in infants

1985 ◽  
Vol 59 (3) ◽  
pp. 847-852 ◽  
Author(s):  
W. A. Carlo ◽  
M. J. Miller ◽  
R. J. Martin
Keyword(s):  
Total Duration ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Peak Amplitude ◽  
Emg Activity ◽  
Inspiratory Time ◽  
Surface Electrodes ◽  
Airway Occlusion ◽  
The Right ◽  
Respiratory Muscle Activity

The effect of end-expiratory occlusion on respiratory muscle activity was studied in 10 unsedated preterm infants during sleep. Electromyograms (EMG) of the upper airway were recorded from surface electrodes placed over the submental (SM) area; diaphragm (DIA) EMGs were obtained with identical electrodes over the right subcostal margin. Phasic SM EMG accompanied 56 +/- 36% of breaths during spontaneous breathing and increased to 80 +/- 26% (P less than 0.05) on the first inspiratory effort after occlusion. Occlusion increased peak amplitude (P less than 0.001) and total duration (P less than 0.005) of the SM EMG without significant changes in its initial rate of rise. In contrast, only the total duration of the DIA EMG increased (P less than 0.005) during occlusion. Inspiratory time increased from 470 +/- 120 to 720 +/- 210 ms (P less than 0.001) during the first occluded effort, but expiratory time did not change. With sustained occlusion, peak amplitude of the SM EMG progressively increased, but DIA EMG only significantly increased by the third occluded effort. Pharyngeal patency was invariably maintained throughout the induced airway occlusions. Sharp bursts of SM EMG activity coincided with resolution of spontaneous obstructive apneic episodes in four infants. The immediate increase in SM EMG associated with airway occlusion may be a mechanism that prevents the development of obstructive apnea.

Regulation of frequency and depth of breathing during expiratory threshold loading in cats

1975 ◽  
Vol 38 (5) ◽  
pp. 869-874 ◽  
Author(s):  
M. M. Grunstein ◽  
I. Wyszogrodski ◽  
J. Milic-Emili
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
The Other ◽  
Spontaneous Ventilation ◽  
Volume Changes ◽  
Phasic Component ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
The Absolute ◽  
Spontaneously Breathing

In six spontaneously breathing anesthetized cats, intermittently subjected to inspiratory elastic loads, we have studied the relationships between tidal volume (VT) and the durations of inspiration (Ti) and breath duration (Ttot) obtained during spontaneous ventilation from resting lung volume (FRCc) and from elevated end-expiratory levels. The latter was elevated by submerging the expiratory breathing line into a column of water, representing the addition of an expiratory threshold load (ETL). The VT vs. Ti relationships obtained at different end-expiratory levels were similar, indicating that during ETL the vagal mechanism regulating Ti responds only to lung volume changes above the new end-expiratory level and is independent of the absolute end-expiratory lung volume. Single vagal fiber recordings suggest that this effect on Ti control may be explained on the basis of adaptation occurring at the level of the pulmonary stretch receptors. The control of Ttot, on the other hand, was found to depend both on the Ti of the preceding breath (phasic component) and on a separate vagal mechanism specifically affecting the duration of expiration (Te) in response to changes in the absolute end-expiratory lung volume. The latter mechanism is functionally inoperative at FRCc.

Pulmonary stretch receptor discharge patterns in eupnea, hypercapnia, and hypoxia

1982 ◽  
Vol 53 (2) ◽  
pp. 346-354 ◽  
Author(s):  
S. Iscoe
Keyword(s):  
Tidal Volume ◽  
Linear Equations ◽  
Discharge Frequency ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Residual Capacity ◽  
Instantaneous Discharge ◽  
Discharge Patterns ◽  
Spontaneously Breathing ◽  
Pulmonary Stretch Receptor

The discharge properties of pulmonary stretch receptors (PSR) were studied in spontaneously breathing, pentobarbital sodium-anesthetized cats. During eupneic breathing, 105 of 116 PSR (both tonically and phasically active) were recruited in the first third of inspiration; none were recruited in the last third. Linear equations adequately expressed the relation between instantaneous discharge frequency and inspired volume in eupnea. During CO2 rebreathing, both tidal volume and peak PSR discharge frequency were inversely related to inspiratory duration. At fixed volumes less than 40 ml above functional residual capacity, instantaneous PSR discharge frequency either did not change or decreased with increases in flow. Above 40 ml, increases in discharge frequency accompanied increases in flow (0.033 spikes/s per ml/s). During progressive hypocapnic hypoxia, discharge frequency increased, on average, at all volumes with increases in flow (0.206 spikes/s per ml/s). During both conditions, as with eupnea, increases in frequency were linearly related to increments in tidal volume. Therefore, tidal volume alone can be used to estimate PSR feedback to the respiratory centers, provided that its instantaneous value is appropriately scaled to account for the different effects of CO2 and hypocapnic hypoxia on PSR discharge.

Influence of CPAP on reflex responses to tracheal irritation in anesthetized humans

1989 ◽  
Vol 67 (3) ◽  
pp. 954-958 ◽  
Author(s):  
T. Nishino ◽  
K. Sugimori ◽  
K. Hiraga ◽  
Y. Hond
Keyword(s):  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Lung Inflation ◽  
Cough Reflex ◽  
Reflex Responses ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Spontaneously Breathing ◽  
Different Levels ◽  
Reflex Cough

We investigated the effects of lung inflation during continuous positive airway pressure breathing (CPAP) on airway defensive reflexes in 10 enflurane-anesthetized spontaneously breathing humans. The airway defensive reflexes were induced by instillation into the trachea of 0.5 ml of distilled water at two different levels of end-expiratory pressure (0 and 10 cmH2O CPAP). The tracheal irritation at an end-expiratory pressure of 0 cmH2O caused a variety of reflex responses including apnea, spasmodic panting, expiration reflex, cough reflex, an increase in heart rate, and an increase in blood pressure. Lung inflation during CPAP of 10 cmH2O did not exert any influence on these reflex responses in terms of the types, latencies, and durations of reflex responses although the intensity of the expiration reflex and cough reflex was augmented by lung inflation. Our results suggest that the pulmonary stretch receptors do not play an important role in the mechanisms of airway defensive reflexes in humans.

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