Upper airway negative-pressure effects on respiratory activity of upper airway muscles

1984 ◽  
Vol 56 (2) ◽  
pp. 500-505 ◽  
Author(s):  
O. P. Mathew

Influence of upper airway negative-pressure change on the respiratory activity of various upper airway muscles was investigated in 13 anesthetized rabbits. Phasic inspiratory activity increased or appeared during virtually all negative-pressure trials in nasolabial, cricothyroid, and posterior cricoarytenoid muscles. No phasic inspiratory activity was seen in the sternothyroid (ST) and sternohyoid (SH) muscles before negative-pressure applications but appeared during 80% of trials in ST and 62% of trials in SH. During maintained negative pressure, a gradual decline in activity was often observed in the nasolabial and laryngeal muscles, whereas a rapid decline in activity was seen in the cervical strap muscles. Reflex effects of negative pressure was markedly reduced or abolished by sectioning the internal branch of the superior laryngeal nerve bilaterally. Reflex augmentation of upper airway muscle activity reported here may have functional significance in the maintenance of upper airway patency. It could prevent upper airway collapse when negative pressure swings in the upper airway increase or facilitate recovery when large negative pressure swings are produced by obstructed inspiratory efforts.

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)


1994 ◽  
Vol 76 (6) ◽  
pp. 2720-2725 ◽  
Author(s):  
T. K. Ghosh ◽  
O. P. Mathew

Effects of intralaryngeal CO2 on the response of superior laryngeal afferents to negative pressure were investigated in 20 anesthetized spontaneously breathing adult cats. Single-fiber action potentials were recorded from the peripheral cut end of the superior laryngeal nerve. The larynx was exposed to negative pressure during inspiration when the animal breathed against an occluded upper airway. Among the 99 receptors evaluated, 54 were respiratory modulated and 45 were nonmodulated endings. The effect of intralaryngeal CO2 on the response of 39 receptors responding to negative pressure was determined by exposure of the larynx to CO2 or air for 1 min followed immediately by upper airway occlusion. The mean discharge frequency of 22 fibers inhibited by negative pressure was 32.4 +/- 2.6 Hz during air trials compared with 29.9 +/- 2.6 Hz during CO2 trials (P < 0.005). During occlusion of the upper airway after the warm humidified air trial, the discharge frequency of these endings decreased to 24.2 +/- 2.3 Hz compared with 17.5 +/- 2.2 Hz after CO2 trial (P < 0.001). The mean discharge frequencies of 17 fibers stimulated by negative pressure were 3.7 +/- 2.6 and 4.4 +/- 1.8 Hz, respectively, during air and CO2 trials. The mean frequencies increased to 14.7 +/- 3.5 Hz (air) and 18.6 +/- 4.0 Hz (CO2) during upper airway occlusions (P < 0.01). We conclude that intralaryngeal CO2 can alter the response of pressure-sensitive laryngeal afferents, thereby having a role in the maintenance of upper airway patency.(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 79 (2) ◽  
pp. 448-454 ◽  
Author(s):  
I. L. Mortimore ◽  
R. Mathur ◽  
N. J. Douglas

Sleep apnea is worse in the supine posture and is associated with retropalatal airway narrowing or occlusion. We have, therefore, examined the effects of posture, negative pressure, and route of respiration on palatal muscle activity in 13 nonsnoring awake male subjects by using electromyography. Electromyographic activity of the levator palatini and palatoglossus was expressed as a percentage of maximum activity. Both the levator palatini (P = 0.002) and palatoglossus (P = 0.002) exhibited phasic inspiratory activity. Overall, posture did not affect the levator palatini (F = 1.58; P = 0.23) or palatoglossus (F = 0.98; P = 0.34) activity, but analysis by route of respiration showed the palatoglossus to be more active when the subjects were nose breathing supine (F = 6.64; P = 0.02). Levator palatini activity was lower when nose breathing was compared with mouth breathing in both the erect and supine postures (F = 6.67; P < 0.02). Nose breathing with the mouth held open caused an increase in palatoglossal activity (P = 0.04). Negative-pressure application (0 to -12.5 cmH2O) caused significant increases in levator palatini (P < 0.001) and palatoglossus (P < 0.001) activity, 100 ms after pressure stimulus, irrespective of route. However, the palatoglossus required significantly greater negative pressures to cause activation when applied via the nose compared with the mouth (P < 0.05). These observations indicate that the levator palatini and palatglossus have respiratory activity and are reflexly activated by negative pressure.


1997 ◽  
Vol 83 (6) ◽  
pp. 1890-1899 ◽  
Author(s):  
Steven W. Mifflin

Mifflin, Steven W. Intensity and frequency dependence of laryngeal afferent inputs to respiratory hypoglossal motoneurons. J. Appl. Physiol. 83(6): 1890–1899, 1997.—Inspiratory hypoglossal motoneurons (IHMs) mediate contraction of the genioglossus muscle and contribute to the regulation of upper airway patency. Intracellular recordings were obtained from antidromically identified IHMs in anesthetized, vagotomized cats, and IHM responses to electrical activation of superior laryngeal nerve (SLN) afferent fibers at various frequencies and intensities were examined. SLN stimulus frequencies <2 Hz evoked an excitatory-inhibitory postsynaptic potential (EPSP-IPSP) sequence or only an IPSP in most IHMs that did not change in amplitude as the stimulus was maintained. During sustained stimulus frequencies of 5–10 Hz, there was a reduction in the amplitude of SLN-evoked IPSPs with time with variable changes in the EPSP. At stimulus frequencies >25 Hz, the amplitude of EPSPs and IPSPs was reduced over time. At a given stimulus frequency, increasing stimulus intensity enhanced the decay of the SLN-evoked postsynaptic potentials (PSPs). Frequency-dependent attenuation of SLN inputs to IHMs also occurred in newborn kittens. These results suggest that activation of SLN afferents evokes different PSP responses in IHMs depending on the stimulus frequency. At intermediate frequencies, inhibitory inputs are selectively filtered so that excitatory inputs predominate. At higher frequencies there was no discernible SLN-evoked PSP temporally locked to the SLN stimuli. Alterations in SLN-evoked PSPs could play a role in the coordination of genioglossal contraction during respiration, swallowing, and other complex motor acts where laryngeal afferents are activated.


1992 ◽  
Vol 73 (3) ◽  
pp. 832-836 ◽  
Author(s):  
S. Zhang ◽  
O. P. Mathew

Negative pressure applied to the upper airway has an excitatory effect on the activity of upper airway muscles and an inhibitory effect on thoracic inspiratory muscles. The role of lung volume feedback in this response was investigated in 10 anesthetized spontaneously breathing adult rabbits. To alter lung volume feedback, the lower airway was exposed to SO2 (250 ppm for 15 min), thereby blocking slowly adapting receptors (SARs). Negative pressure pulses (5, 10, and 20 cmH2O, 300-ms duration) were applied to the functionally isolated upper airway before and after SAR blockade. Tracheal airflow and electromyogram (EMG) of the genioglossus and alae nasi were recorded. Peak EMG, peak inspiratory flow, tidal volume, and respiratory timing of control breaths (3 breaths immediately preceding test) and test breaths were determined. Analysis of variance was used to determine the significance of the effects. Negative pressure pulses increased peak EMG of genioglossus and alae nasi and inspiratory duration and decreased peak inspiratory flow. These effects were larger after SAR blockade. We conclude that a decrease in volume feedback from the lung augments the response to upper airway pressure change.


1987 ◽  
Vol 63 (1) ◽  
pp. 229-237 ◽  
Author(s):  
E. van Lunteren

The interactive effects of upper airway negative pressure and hypercapnia on the pattern of breathing were assessed in pentobarbital-anesthetized cats. At any given level of pressure in the upper airway, hypercapnia increased respiratory rate, reduced inspiratory time, and augmented tidal volume, inspiratory airflow, and the peak and rate of rise of diaphragm electrical activity. Conversely, at any given level of CO2, upper airway negative pressure decreased respiratory rate, prolonged inspiratory time, and depressed inspiratory airflow and diaphragm electromyogram (EMG) rate of rise. Application of negative pressure to the upper airway shifted the relationship between tidal volume and inspiratory time upward and rightward. The relationship between inspiratory and expiratory times, however, was linearly correlated over a wide range of chemical drives and levels of upper airway pressure. These results suggest that in the anesthetized cat upper airway negative pressure afferent inputs 1) interact in an additive fashion with hypercapnia to alter the pattern of breathing, 2) interact multiplicatively with CO2 to influence mean inspiratory airflow and diaphragm EMG rate of rise, 3) depress the generation of central inspiratory activity, 4) increase the time-dependent volume threshold for inspiratory termination, and 5) affect the ratio between inspiratory and expiratory times in a similar manner as alterations in PCO2.


1988 ◽  
Vol 65 (1) ◽  
pp. 205-209 ◽  
Author(s):  
D. L. Woodall ◽  
O. P. Mathew

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.


2002 ◽  
Vol 92 (1) ◽  
pp. 269-278 ◽  
Author(s):  
Stephen Ryan ◽  
Walter T. McNicholas ◽  
Ronan G. O'Regan ◽  
Philip Nolan

10.1152/japplphysiol.00413.2001.—Distortion of the upper airway by negative transmural pressure (UANP) causes reflex vagal bradycardia. This requires activation of cardiac vagal preganglionic neurons, which exhibit postinspiratory (PI) discharge. We hypothesized that UANP would also stimulate cranial respiratory motoneurons with PI activity. We recorded 32 respiratory modulated motor units from the recurrent laryngeal nerve of seven decerebrate paralyzed rabbits and recorded their responses to UANP and to withholding lung inflation using a phrenic-triggered ventilator. The phasic inspiratory ( n = 17) and PI ( n = 5) neurons detected were stimulated by −10 cmH2O UANP and by withdrawal of lung inflation ( P < 0.05, Friedman's ANOVA). Expiratory-inspiratory units ( n = 10) were tonically active but transiently inhibited in postinspiration; this inhibition was more pronounced and prolonged during UANP stimuli and during no-inflation tests ( P < 0.05). We conclude that, in addition to increasing inspiratory activity in the recurrent laryngeal nerve, UANP also stimulates units with PI activity.


1998 ◽  
Vol 84 (4) ◽  
pp. 1299-1304 ◽  
Author(s):  
Franca B. Sant’Ambrogio ◽  
Giuseppe Sant’Ambrogio ◽  
Kyungsoon Chung

Gastroesophageal reflux has been indicated as an etiopathological factor in disorders of the upper airway. Upper airway collapsing pressure stimulates pressure-responsive laryngeal receptors that reflexly increase the activity of upper airway abductor muscles. We studied, in anesthetized dogs, the effects of repeated laryngeal instillations of HCl-pepsin (HCl-P; pH = 2) on the response of laryngeal afferent endings and the posterior cricoarytenoid muscle (PCA) to negative pressure. The effect of negative pressure on receptor discharge or PCA activity was evaluated by comparing their response to upper airway (UAO) and tracheal occlusions (TO). It is only during UAO, but not during TO, that the larynx is subjected to negative transmural pressure. HCl-P instillation decreased the rate of discharge during UAO of the 10 laryngeal receptors studied from 56.4 ± 10.9 (SE) to 38.2 ± 9.2 impulses/s ( P < 0.05). With UAO, the peak PCA moving time average, normalized by dividing it by the peak values of esophageal pressure, decreased after six HCl-P trials from 4.29 ± 0.31 to 2.23 ± 0.18 ( n = 6; P < 0.05). The responses to TO of either receptors or PCA remained unaltered. We conclude that exposure of the laryngeal mucosa to HCl-P solutions, as it may occur with gastroesophageal reflux, impairs the patency-maintaining mechanisms provided by laryngeal sensory feedback. Inflammatory and necrotic alterations of the laryngeal mucosa are likely responsible for these effects.


1998 ◽  
Vol 85 (3) ◽  
pp. 1135-1141 ◽  
Author(s):  
A. Bradford ◽  
D. McKeogh ◽  
R. G. O’Regan

We compared the effects of CO2 applied continuously and during expiration on laryngeal-receptor activity in paralyzed, artificially ventilated and nonparalyzed, spontaneously breathing cats by using an isolated larynx, artificially ventilated to approximate a normal respiratory cycle. The majority of quiescent negative-pressure and all cold receptors were excited by 5 and 9% CO2 applied both continuously and during expiration. In general, quiescent positive-pressure, tonic negative-pressure, and tonic positive-pressure receptors were inhibited by 5 and 9% CO2 applied continuously and during expiration. There were no significant differences between responses to 5 and 9% CO2 or to continuous and expired CO2 or between paralyzed and nonparalyzed preparations. In conclusion, laryngeal receptors respond to changes in CO2 concentration occurring during a normal respiratory cycle. Because laryngeal-receptor stimulation exerts reflex effects on ventilation and upper airway muscle activity, these results suggest that airway CO2 plays a role in reflex regulation of breathing and upper airway patency.


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