Reflex control of expiratory airflow and duration

1977 ◽  
Vol 42 (1) ◽  
pp. 80-87 ◽  
Author(s):  
J. E. Remmers ◽  
D. Bartlett
Keyword(s):  
Respiratory Muscle ◽  
Time Course ◽  
Airway Resistance ◽  
Upper Airway ◽  
Pressure Measurements ◽  
Airway Occlusion ◽  
Tracheal Pressure ◽  
Expiratory Muscles ◽  
Reflex Control ◽  
Emg Electrodes

Unanesthetized, unrestrained cats were studied repeatedly after placement of a permanent tracheostomy, catheters for respiratory pressure measurements, and respiratory muscle EMG electrodes. The tracheostomy was opened or closed by a remote mechanism. Opening the tracheostomy reduced tracheal pressure to zero and diverted flow from the upper airway; closing the tracheostomy reestablished the normal pathway for airflow. Opening the tracheostomy during expiration evoked reflex responses in the diaphragm, in the laryngeal abductor and in abdominal expiratory muscles. These were sustained compensatory (“tracking”) responses which, in each case, acted to offset loss of expiratory braking by the upper airway. Occlusion of the tracheostomy during expiration produced the opposite responses. Responses to tracheostomy opening usually overcompensated for the loss of upper airway resistance, suggesting that extrathoracic tracheal receptors may participate in tracking. Changes in the expiratory time course of lung volume were accompanied by changes in the duration of expiration. These “triggering” responses were shown to operate independently of the tracking responses though both were eliminated by vagotomy.

scholarly journals Geniohyoid muscle function in awake canines

2003 ◽  
Vol 95 (2) ◽  
pp. 810-817 ◽  
Author(s):  
M. Yokoba ◽  
H. G. Hawes ◽  
P. A. Easton
Keyword(s):  
Muscle Function ◽  
Breathing Pattern ◽  
Muscle Length ◽  
Upper Airway ◽  
Mechanical Action ◽  
Emg Activity ◽  
Airway Occlusion ◽  
Lateral Decubitus ◽  
The Right ◽  
Emg Electrodes

The geniohyoid (Genio) upper airway muscle shows phasic, inspiratory electrical activity in awake humans but no activity and lengthening in anesthetized cats. There is no information about the mechanical action of the Genio, including length and shortening, in any awake, nonanesthetized mammal during respiration (or swallowing). Therefore, we studied four canines, mean weight 28.8 kg, 1.5 days after Genio implantation with sonomicrometry transducers and bipolar electromyogram (EMG) electrodes. Awake recordings of breathing pattern, muscle length and shortening, and EMG activity were made with the animal in the right lateral decubitus position during quiet resting, CO2-stimulated breathing, inspiratory-resisted breathing (80 cmH2O · l-1 · s), and airway occlusion. Genio length and activity were also measured during swallowing, when it shortened, showing a 9.31% change from resting length, and its EMG activity increased 6.44 V. During resting breathing, there was no phasic Genio EMG activity at all, and Genio showed virtually no movement during inspiration. During CO2-stimulated breathing, Genio showed minimal lengthening of only 0.07% change from resting length, whereas phasic EMG activity was still absent. During inspiratory-resisted breathing and airway occlusion, Genio showed phasic EMG activity but still lengthened. We conclude that the Genio in awake, nonanesthetized canines shows active contraction and EMG activity only during swallowing. During quiet or stimulated breathing, Genio is electrically inactive with passive lengthening. Even against resistance, Genio is electrically active but still lengthens during inspiration.

Late response of the upper airway of the rat to inhaled antigen

1990 ◽  
Vol 69 (4) ◽  
pp. 1360-1365 ◽  
Author(s):  
L. J. Xu ◽  
D. H. Eidelman ◽  
J. H. Bates ◽  
J. G. Martin
Keyword(s):  
Time Course ◽  
Airway Resistance ◽  
Upper Airway ◽  
Brown Norway ◽  
Control Group ◽  
Late Response ◽  
Lung Elastance ◽  
Upper Airway Resistance ◽  
Airway Responses ◽  
Peak Value

We studied the magnitude and time course of changes in upper airway resistance (Ruaw) of actively sensitized Brown-Norway rats after aerosol challenge with ovalbumin (OA). Two weeks after sensitization, eight rats were challenged by inhalation of aerosolized OA through the nose. The airway responses of these rats 5-10 h after OA challenge were compared with those of seven animals challenged with saline. Seven of eight test rats had increased Ruaw, and six displayed discrete late responses (LR). Ruaw during expiration was highly alinear so analysis was confined to Ruaw during inspiration (Ruaw,I). The Ruaw,I averaged over 5 h was 1.262 +/- 0.09 (SE) cmH2O.ml-1.s, 2.6 times the value for saline-challenged animals (0.476 +/- 0.143 cmH2O.ml-1.s), and it reached a peak value of 3.454 +/- 0.45 cmH2O.ml-1.s. The time to the peak of the LR was 446 +/- 37.3 min. The duration of the LR in the upper airway was 146 +/- 34.9 min. At the time corresponding to the peak value of Ruaw,I, the lung elastance in the test rats was double the value preceding the peak. Lung elastance was unchanged in the control group. We conclude that inhalation of antigen through the upper airway of the sensitized rat results in a substantial increase in upper airway resistance and a distinct LR. The predominant site of the change in respiratory system resistance is in the upper airway.

Load compensation and respiratory muscle function during sleep

1992 ◽  
Vol 72 (4) ◽  
pp. 1221-1234 ◽  
Author(s):  
K. G. Henke ◽  
M. S. Badr ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Chest Wall ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Airway Resistance ◽  
Upper Airway ◽  
Rapid Eye Movement Sleep ◽  
Compensatory Mechanisms ◽  
Ventilatory Control ◽  
Load Compensation

The sleeping state places unique demands on the ventilatory control system. The sleep-induced increase in airway resistance, the loss of consciousness, and the need to maintain the sleeping state without frequent arousals require the presence of complex compensatory mechanisms. The increase in upper airway resistance during sleep represents the major effect of sleep on ventilatory control. This occurs because of a loss of muscle activity, which narrows the airway and also makes it more susceptible to collapse in response to the intraluminal pressure generated by other inspiratory muscles. The magnitude and timing of the drive to upper airway vs. other inspiratory pump muscles determine the level of resistance and can lead to inspiratory flow limitation and complete upper airway occlusion. The fall in ventilation with this mechanical load is not prevented, as it is in the awake state, because of the absence of immediate compensatory responses during sleep. However, during sleep, compensatory mechanisms are activated that tend to return ventilation toward control levels if the load is maintained. Upper airway protective reflexes, intrinsic properties of the chest wall, muscle length-compensating reflexes, and most importantly chemoresponsiveness of both upper airway and inspiratory pump muscles are all present during sleep to minimize the adverse effect of loading on ventilation. In non-rapid-eye-movement sleep, the high mechanical impedance combined with incomplete load compensation causes an increase in arterial PCO2 and augmented respiratory muscle activity. Phasic rapid-eye-movement sleep, however, interferes further with effective load compensation, primarily by its selective inhibitory effects on the phasic activation of postural muscles of the chest wall. The level and pattern of ventilation during sleep in health and disease states represent a compromise toward the ideal goal, which is to achieve maximum load compensation and meet the demand for chemical homeostasis while maintaining sleep state.

Role of carotid sinus and aortic nerves in respiratory control of infant rats

1986 ◽  
Vol 251 (4) ◽  
pp. R811-R817 ◽  
Author(s):  
M. A. Hofer
Keyword(s):  
Airway Obstruction ◽  
Carotid Sinus ◽  
Respiratory Control ◽  
Upper Airway ◽  
Airway Occlusion ◽  
Infant Rats ◽  
Tracheal Pressure ◽  
Recovery Times ◽  
Prolonged Recovery ◽  
Low Amplitude

The roles of carotid sinus (CSN) and aortic depressor nerves (ADN) in the maintenance of rhythmic respiration and in the response to airway occlusion were investigated in 8- to 10-day-old infant rats. Cutting the CSN led to a periodic loss of rhythmic respiration with arrhythmic low-amplitude waveforms, frequent end-expiratory pauses, and occasional apneas observed in unanesthetized unrestrained pups studied in their home cage nests by impedance pneumography. Cutting the ADN alone did not have this effect. Sinoaortic denervation (SAD) in which both nerves were cut, produced a more severe disturbance that was not relieved by tracheostomy, indicating that it was not due to upper airway obstruction. Tracheal pressure recordings from anesthetized SAD infants in response to short periods of external airway obstruction showed reduced respiratory efforts and prolonged recovery times, deficits that may play a role in the mortality previously reported after SAD in infant rats.

Decay of inspiratory muscle pressure during expiration in anesthetized cats

1983 ◽  
Vol 54 (2) ◽  
pp. 408-413 ◽  
Author(s):  
W. A. Zin ◽  
L. D. Pengelly ◽  
J. Milic-Emili
Keyword(s):  
Respiratory System ◽  
Time Course ◽  
Pentobarbital Sodium ◽  
Airway Occlusion ◽  
Inspiratory Muscles ◽  
Tracheal Pressure ◽  
Resistive Loads ◽  
The Moment ◽  
Spontaneously Breathing

In six spontaneously breathing anesthetized cats (pentobarbital sodium, 35 mg/kg) we studied the antagonistic pressure developed by the inspiratory muscles during expiration (PmusI). This was accomplished in two ways: 1) with our previously reported method (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 1266–1271, 1982) based on the measurement of changes in lung volume and airflow during spontaneous expiration, together with determination of the total passive respiratory system elastance and resistance; and 2) measurement of the time course of changes in tracheal/pressure after airway occlusion at end inspiration, up to the moment when the inspiratory muscles become completely relaxed. The agreement between the two methods is generally good, both in the amplitude of PmusI and in its time course. We also applied the first method to spontaneous expirations through added linear resistive loads. These did not alter the relative decay of PmusI. Thus in anesthetized cats the braking action of the inspiratory muscles does not decrease when expiratory resistive loads are added, i.e., when such braking is clearly not required.

Effects of raising carotid sinus pressure on upper airway resistance and EEG frequency in sleeping dogs

1995 ◽  
Vol 78 (5) ◽  
pp. 1699-1709 ◽  
Author(s):  
K. W. Saupe ◽  
C. A. Smith ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Airway Resistance ◽  
Carotid Sinus ◽  
Cardiovascular Response ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Consistent Finding ◽  
Upper Airway Resistance ◽  
Tracheal Pressure ◽  
Baroreceptor Stimulation ◽  
Sinus Pressure

The purpose of this study was to determine whether acutely raising carotid sinus pressure (Pcs) causes changes in upper airway resistance and/or electroencephalographic (EEG) frequency during wakefulness and non-rapid-eye-movement (NREM) sleep. Five dogs were chronically instrumented so that breathing, tracheal pressure, mouth pressure, EEG, and electrooculogram could be measured while pressure in the vascularly isolated carotid sinus was rapidly increased between 40 and 150 mmHg via an extracorporeal perfusion circuit. Dogs were studied during both wakefulness and NREM sleep. Multiple trials of increased Pcs were conducted in each dog. We observed that increasing Pcs 40–150 mmHg caused not only a reflex cardiovascular response but also a 15–40% decrease in minute ventilation. Raising Pcs caused no physiologically significant changes in upper airway resistance over the range of airway pressures and flow rates encountered during inspiration and expiration. Even dogs that demonstrated moderate to substantial sleep-induced increases in airway resistance did not consistently increase resistance during superimposed baroreceptor stimulation. Small increases in airway resistance were sometimes observed during baroreceptor stimulation, but this was not a consistent finding. Acute increases in Pcs did not cause measurable changes in EEG frequency during wakefulness or NREM sleep. We conclude that acute stimulation of the carotid sinus baroreceptors does not cause physiologically meaningful changes in upper airway resistance or EEG activity in awake or sleeping dogs.

scholarly journals Differential respiratory muscle recruitment induced by clonidine in awake goats

1998 ◽  
Vol 84 (4) ◽  
pp. 1198-1207 ◽  
Author(s):  
Michael S. Hedrick ◽  
Melinda R. Dwinell ◽  
Patrick L. Janssen ◽  
Josue Pizarro ◽  
Gerald E. Bisgard
Keyword(s):  
Respiratory Muscle ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Transversus Abdominis ◽  
Muscle Recruitment ◽  
Breathing Cycle ◽  
Peripheral Chemoreceptor ◽  
Inspiratory Muscles ◽  
Tonic Activation ◽  
Expiratory Muscles

The purpose of this study was to test the hypothesis that dysrhythmic breathing induced by the α2-agonist clonidine is accompanied by differential recruitment of respiratory muscles. In adult goats ( n = 14) electromyographic (EMG) measurements were made from inspiratory muscles (diaphragm and parasternal intercostal) and expiratory muscles [triangularis sterni (TS) and transversus abdominis (Abd)]. EMG of the thyroarytenoid (TA) muscle was used as an index of upper airway (glottal) patency. Peak EMG activities of all spinal inspiratory and expiratory muscles were augmented by central and peripheral chemoreceptor stimuli. Phasic TA was apparent in the postinspiratory phase of the breathing cycle under normoxic conditions. During dysrhythmic breathing episodes induced by clonidine, TS and Abd activities were attenuated or abolished, whereas diaphragm and parasternal intercostal activities were unchanged. There was no tonic activation of TS or Abd EMG during apneas; however, TA activity became tonic throughout the apnea. We conclude that 1) α2-adrenoceptor stimulation results in differential recruitment of respiratory muscles during respiratory dysrhythmias and 2) apneas are accompanied by active glottic closure in the awake goat.

scholarly journals Upper airway pressure-flow relationships and pharyngeal constrictor EMG activity during prolonged expiration in awake goats

2008 ◽  
Vol 105 (1) ◽  
pp. 100-108
Author(s):  
K. D. O'Halloran ◽  
G. E. Bisgard
Keyword(s):  
Airway Pressure ◽  
Muscle Activation ◽  
Upper Airway ◽  
Systemic Administration ◽  
Emg Activity ◽  
Airway Closure ◽  
Pressure Flow ◽  
Airway Occlusion ◽  
Adductor Muscles ◽  
Tracheal Pressure

We undertook the present investigation to establish whether narrowing/closure of the upper airway occurs during spontaneous and provoked respiratory rhythm disturbances and whether pharyngeal constrictor muscle recruitment occurs coincident with upper airway occlusion during prolonged expiratory periods. Upper airway pressure-flow relationships and middle pharyngeal constrictor (mPC) EMG activities were recorded in 11 adult female goats during spontaneous and provoked prolongations in expiratory time (Te). A total of 213 spontaneous prolongations of expiration were recorded. Additionally, 169 prolonged expiratory events preceded by an augmented breath were included in the analyses. In separate trials on different days, Te was prolonged by systemic administration of dopamine, by raising the inspired fraction of O2 from 0.10 to 1.00 during poikilocapnic conditions or by systemic administration of clonidine. Continuous tonic activation of the mPC EMG was observed during each prolonged Te period regardless of the duration or initiating cause. However, significant increases in subglottic tracheal pressure, with expiratory airflow braking indicative of upper airway narrowing or closure, was only observed during spontaneous events without a preceding augmented breath and during clonidine-induced events. Tonic mPC activation proved an unreliable indicator of airway occlusion. Furthermore, mPC muscle activation alone is not sufficient to induce pharyngeal occlusion during prolonged expiration. Our data suggest that airway closure is not a common occurrence during provoked respiratory disturbances in awake goats. We propose that airway closure, when present during prolonged Te, is more likely dependent on activation of laryngeal adductor muscles with glottic braking independent of pharyngeal narrowing.

Reflex control of diaphragm activation by thoracic afferents

1993 ◽  
Vol 75 (1) ◽  
pp. 63-69 ◽  
Author(s):  
J. R. Romaniuk ◽  
G. S. Supinski ◽  
A. F. DiMarco
Keyword(s):  
Lung Volume ◽  
Airway Pressure ◽  
Respiratory Muscle ◽  
Motor Response ◽  
Airway Occlusion ◽  
Thoracic Level ◽  
Complete Section ◽  
Residual Capacity ◽  
Reflex Control ◽  
The Relationship

Recent studies suggest that chest wall reflexes may have a role in modulating diaphragm activation. The purpose of this study was to more closely examine this issue by assessing the diaphragmatic motor response to airway occlusion. Studies were performed in vagotomized mongrel dogs anesthetized with pentobarbital sodium. Diaphragmatic electromyogram (EMG) and phrenic neurogram (ENG) responses to airway occlusion were evaluated at different precontractile respiratory muscle lengths, achieved by passive inflation and deflation with a volume syringe during the preceding expiration. Lung volume was expressed as the corresponding change in airway pressure. At functional residual capacity, deflation (-5 cmH2O), and large inflation (+25 cmH2O), phrenic ENG during occlusion was 90 +/- 2 (SE), 84 +/- 5, and 86 +/- 3% of the preceding control breaths, respectively (n = 9). Qualitatively similar, but somewhat more pronounced, responses were observed on diaphragmatic EMG. With small lung inflations, the degree of reduction of phrenic ENG with airway occlusion was less. Consequently, the relationship between airway pressure and degree of inhibition was best described as a reverse parabola with the maximum at approximately +10–15 cmH2O. Responses were not significantly affected by bilateral cervical phrenicotomy. Complete section of the spinal cord at the high thoracic level (T1-T2) abolished the observed reduction in phrenic ENG in response to airway occlusion. Our results demonstrate 1) the existence of nonvagal nonphrenic reflex control of diaphragm activation most likely secondary to activation of intercostal afferents and 2) that the magnitude of this reflex is highly dependent on factors related to lung volume.

Airway occlusion pressure

1993 ◽  
Vol 74 (4) ◽  
pp. 1475-1483 ◽  
Author(s):  
W. A. Whitelaw ◽  
J. P. Derenne
Keyword(s):  
Chest Wall ◽  
Time Course ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Occlusion Pressure ◽  
Airway Occlusion ◽  
Clinical Investigations ◽  
Proportionate Change ◽  
Phase Lags ◽  
Airway Occlusion Pressure

Airway occlusion pressure has been used in the past two decades for assessing output of the respiratory controller. It gives a measurement of a weighted sum of the effect of all respiratory muscles active at a given time and, unlike ventilation or tidal volume, does not depend on the resistance or compliance of the respiratory system. In anesthetized subjects or animals, it gives a tracing of the time course of respiratory neuromuscular output through the respiratory cycle, modified by elimination of most phasic vagal stretch receptor feedback and perhaps slightly by activation of some chest wall reflexes. The original postulate that an occluded inspiration would be isometric and the measured pressure free from losses due to force-length and force-velocity has been shown to be incorrect. The volume at which occlusion takes effect, distortions of the chest wall during the maneuver, tonic vagal input, and strength of the muscles must be taken into account when the data are interpreted. Brief occlusions [pressure at 0.1 s (P0.1)] are useful in measuring output in the very first part of inspiration in conscious subjects but must be treated with a great deal of caution. They are most reliable when end-expiratory volume remains constant and there are no important phase lags between flow and pressure. Allowance may be necessary for damping of the pressure signal on its passing through the compliant upper airway. Changes in P0.1 may often be due to changes in the shape of the driving pressure wave without a proportionate change in overall output. The technique remains useful when its limitations are recognized. Because of its simplicity, it can be easily and usefully applied to a range of clinical investigations.

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