Differential suppression of upper airway motor activity during carbachol-induced, REM sleep-like atonia

1998 ◽  
Vol 275 (4) ◽  
pp. R1013-R1024 ◽  
Author(s):  
Victor Fenik ◽  
Richard O. Davies ◽  
Allan I. Pack ◽  
Leszek Kubin
Keyword(s):  
Motor Activity ◽  
Eye Movement ◽  
Rem Sleep ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Laryngeal Nerve ◽  
Pharyngeal Branch ◽  
Induced Changes ◽  
Upper Airway Muscles ◽  
Decerebrate Cats

Microinjections of carbachol into the pontine tegmentum of decerebrate cats have been used to study the mechanisms underlying the suppression of postural and respiratory motoneuronal activity during the resulting rapid eye movement (REM) sleep-like atonia. During REM sleep, distinct respiratory muscles are differentially affected; e.g., the activity of the diaphragm shows little suppression, whereas the activity of some upper airway muscles is quite strong. To determine the pattern of the carbachol-induced changes in the activity of different groups of upper airway motoneurons, we simultaneously recorded the efferent activity of the recurrent laryngeal nerve (RL), pharyngeal branch of the vagus nerve (Phar), and genioglossal branch of the hypoglossal (XII) and phrenic (Phr) nerves in 12 decerebrate, paralyzed, vagotomized, and artificially ventilated cats. Pontine carbachol caused a stereotyped suppression of the spontaneous activity that was significantly larger in Phar expiratory (to 8.3% of control) and XII inspiratory motoneurons (to 15%) than in Phr inspiratory (to 87%), RL inspiratory (to 79%), or RL expiratory motoneurons (to 72%). The suppression in upper airway motor output was significantly greater than the depression caused by a level of hypocapnia that reduced Phr activity as much as carbachol. We conclude that pontine carbachol evokes a stereotyped pattern of suppression of upper airway motor activity. Because carbachol evokes a state having many neurophysiological characteristics similar to those of REM sleep, it is likely that pontine cholinoceptive neurons have similar effects on the activity of upper airway motoneurons during both states.

Control of Upper Airway Motoneurons During REM Sleep

Physiology ◽  
1998 ◽  
Vol 13 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Leszek Kubin ◽  
Richard O. Davies ◽  
Allan I. Pack
Keyword(s):  
Animal Model ◽  
Eye Movement ◽  
Rem Sleep ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
State Dependent ◽  
Dependent Inhibition ◽  
Upper Airway Muscles

The loss of tone in upper airway muscles contributes to disorders of breathing during sleep. In an animal model of rapid eye movement sleep atonia, decrements in the activity of upper airway motoneurons are caused by withdrawal of excitation mediated by serotonin and other transmitters, rather than by state-dependent inhibition.

Respiratory muscle responses to changes in chemoreceptor drive in infants

1990 ◽  
Vol 68 (3) ◽  
pp. 1041-1047 ◽  
Author(s):  
W. A. Carlo ◽  
J. M. DiFiore
Keyword(s):  
Preterm Infants ◽  
Respiratory Muscle ◽  
Muscle Activation ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Obstructive Apnea ◽  
Surface Electrodes ◽  
Posterior Cricoarytenoid ◽  
Upper Airway Muscles ◽  
Muscle Responses

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.

Negative pressure-induced deformation of the upper airway causes central apnea in awake and sleeping dogs

1996 ◽  
Vol 80 (5) ◽  
pp. 1528-1539 ◽  
Author(s):  
C. A. Harms ◽  
Y. J. Zeng ◽  
C. A. Smith ◽  
E. H. Vidruk ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Negative Pressure ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Electromyographic Activity ◽  
Rapid Eye Movement ◽  
Topical Anesthetic ◽  
Control Value ◽  
States Of Consciousness

We investigated the effects of negative pressure (NP) in the isolated upper airway (UA) in three unanesthetized dogs. The UA was isolated, and the dogs breathed through an endotracheal tube while wearing a fitted fiberglass snout mask. NP (-2 to -32 cmH2O) was applied in a square wave below the larynx or at the snout at end expiration and was held until inspiratory effort during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep. During all states of consciousness, NP applied to the UA prolonged expiratory time (TE) 1) below a threshold of -8 to -10 cmH2O, which coincided with closure of the oro- and/or velopharynx; and 2) in a progressive fashion at more negative pressures than threshold, up to a mean apneic length of 324% of the control value (or 13.9 s) at -30 cmH2O. TE prolongation was less during REM sleep at a given NP (P < 0.05). Augmented tonic genioglossal electromyographic activity also occurred with the applied NP during wakefulness and NREM sleep but not with REM sleep. NP (-20 to -32 cmH2O) applied as a brief pulse (300-500 ms) during NREM sleep caused transient airway occlusion, terminated the breath during inspiration, and prolonged TE when applied at end expiration. Central apneas always persisted beyond the termination of the UA closure. TE prolongation in response to NP persisted in the presence of a topical anesthetic nebulized through the UA sufficient to abolish the laryngeal gag reflexes. We conclude that UA closure and deformation will cause significant TE prolongation during all states of consciousness and activation of the genioglossus muscle during wakefulness and NREM sleep but not during REM sleep.

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.

Nasal and laryngeal reflex responses to negative upper airway pressure

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 ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Muscle Activity ◽  
Moving Average ◽  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Laryngeal Nerve ◽  
Topical Anesthesia ◽  
Inspiratory Activity ◽  
Posterior Cricoarytenoid ◽  
Upper Airway Muscles

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)

Upper airway closing pressures in obstructive sleep apnea

1984 ◽  
Vol 57 (2) ◽  
pp. 520-527 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Eye Movement ◽  
Rem Sleep ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Stage I ◽  
Stage Iii ◽  
Rapid Eye Movement ◽  
Obstructive Sleep

We studied 18 patients with obstructive sleep apnea (OSA). Each subject slept while breathing through the nose with a specially designed valveless breathing circuit. Low levels of continuous positive airway pressure (CPAP) applied through the nose (2.5–15.0 cmH2O) prevented OSA and allowed long periods of stable stage III/IV sleep and rapid-eye-movement (REM) sleep. Externally applied complete nasal occlusion while the upper airway was patent resulted in upper airway closure during inspiration which was identified by a sudden deviation of nasal pressure from tracheal or esophageal pressure. The level of upper airway closing pressure (UACP) did not change throughout the occlusion test, suggesting that upper airway dilator muscles do not respond to asphyxia during sleep. The upper airway was more collapsible during stage I/II non-rapid-eye-movement (NREM) and REM sleep compared with stage III/IV NREM sleep. The pooled mean UACP was 3.1 +/- 0.4 cmH2O in stage I/II NREM, 4.2 +/- 0.2 cmH2O in stage III/IV NREM, and 2.4 +/- 0.2 cmH2O in REM sleep. Nasal occlusion at successively higher levels of CPAP did not alter the level of UACP in stage I/II NREM and REM sleep but resulted in the upper airway becoming more stable in stage III/IV NREM sleep, suggesting a reflex which augments the tone of upper airway dilator muscles.

scholarly journals Coordinated Respiratory Motor Activity in Nerves Innervating the Upper Airway Muscles in Rats

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0166436 ◽  
Author(s):  
Satoshi Tachikawa ◽  
Kiyomi Nakayama ◽  
Shiro Nakamura ◽  
Ayako Mochizuki ◽  
Takehiko Iijima ◽  
...  
Keyword(s):  
Motor Activity ◽  
Upper Airway ◽  
Upper Airway Muscles

Sleep and the ventilatory response to resistive loading in normal men

1988 ◽  
Vol 64 (3) ◽  
pp. 1186-1195 ◽  
Author(s):  
L. Wiegand ◽  
C. W. Zwillich ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Airway Resistance ◽  
Ventilatory Response ◽  
Upper Airway ◽  
Resistive Load ◽  
Load Compensation ◽  
Resistive Loading ◽  
Resistive Loads ◽  
Normal Men

Since upper airway resistance is known to increase during sleep, inadequate resistive load compensation may contribute to the normal decline in sleeping ventilation. We determined the acute and sustained (4 min) ventilatory response to a range of external inspiratory resistive loads (4, 8, 12, and 25 cmH2O.l-1.s) during wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep in seven normal men. We found that minute ventilation (VI) was well maintained with acute and sustained resistive loading during wakefulness. Immediate adjustments in ventilatory timing (prolongation of inspiratory duration) provided full compensation for airflow reduction. In marked contrast, resistive load application during NREM sleep invariably produced a significant (P less than 0.05) reduction in VI with progressively larger resistive loads producing progressively greater ventilatory decrements. This decline in ventilation was a product of a falling inspiratory flow rate with inadequate prolongation of inspiratory duration (TI). The largest decrements in ventilation occurred immediately after load application followed by partial ventilatory recovery, which occurred over time in concert with rising PCO2 and augmented ventilatory effort (as reflected by P0.1 or mouth occlusion pressure). Similar observations were made during REM sleep, although the responses were less consistent and fewer data were obtained. These observations support the hypothesis that poor load compensation for increased upper airway resistance contributes to the hypoventilation characteristic of normal sleep.

scholarly journals The effect of rapid eye movement (REM) sleep on upper airway mechanics in normal human subjects

1998 ◽  
Vol 510 (3) ◽  
pp. 963-976 ◽  
Author(s):  
James A. Rowley ◽  
Brian R. Zahn ◽  
Mark A. Babcock ◽  
M. Safwan Badr
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Human Subjects ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Airway Mechanics ◽  
Normal Human

Response of genioglossus muscle activity to nasal airway occlusion in normal sleeping adults

1988 ◽  
Vol 64 (1) ◽  
pp. 347-353 ◽  
Author(s):  
S. T. Kuna ◽  
J. Smickley
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Muscle Activity ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Mouth Breathing ◽  
Nasal Airway ◽  
Rapid Eye Movement ◽  
Genioglossus Muscle ◽  
Airway Occlusion

To determine the combined effect of increased subatmospheric upper airway pressure and withdrawal of phasic volume feedback from the lung on genioglossus muscle activity, the response of this muscle to intermittent nasal airway occlusion was studied in 12 normal adult males during sleep. Nasal occlusion at end expiration was achieved by inflating balloon-tipped catheters located within the portals of a nose mask. No seal was placed over the mouth. During nose breathing in non-rapid-eye-movement (NREM) sleep, nasal airway occlusion resulted in multiple respiratory efforts before arousal. Mouth breathing was not initiated until arousal. Phasic inspiratory genioglossus activity was present in eight subjects during NREM sleep. In these subjects, comparison of peak genioglossus inspiratory activity on the first three occluded efforts to the value just before occlusion showed an increase of 4.7, 16.1, and 28.0%, respectively. The relative increases in peak genioglossus activity were very similar to respective increases in peak diaphragm activity. Arousal was associated with a large burst in genioglossus activity. During airway occlusion in rapid-eye-movement (REM) sleep, mouth breathing could occur without a change in sleep state. In general, genioglossus responses to airway occlusion in REM sleep were similar in pattern to those in NREM sleep. A relatively small reflex activation of upper airway muscles associated with a sudden increase in subatmospheric pressure in the potentially collapsible segment of the upper airway may help compromise upper airway patency during sleep.

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