Respiratory Activity of the Rat Posterior Cricoarytenoid Muscle

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.

1989 ◽  
Vol 66 (3) ◽  
pp. 1501-1505 ◽  
Author(s):  
G. Insalaco ◽  
G. Sant'Ambrogio ◽  
F. B. Sant'Ambrogio ◽  
S. T. Kuna ◽  
O. P. Mathew

Esophageal electrodes have been used for recording the electromyographic (EMG) activity of the posterior cricoarytenoid muscle (PCA). To determine the specificity of this EMG technique, esophageal electrode recordings were compared with intramuscular recordings in eight anesthetized mongrel dogs. Intramuscular wire electrodes were placed in the right and left PCA, and the esophageal electrode was introduced through the nose or mouth and advanced into the upper esophagus. On direct visualization of the upper airway, the unshielded catheter electrode entered the esophagus on the right or left side. Cold block of the recurrent laryngeal nerve (RLN) ipsilateral to the esophageal electrode was associated with a marked decrease in recorded activity, whereas cold block of the contralateral RLN resulted only in a small reduction in activity. After supplemental doses of anesthesia were administered, bilateral RLN cold block essentially abolished the activity recorded with the intramuscular electrodes as well as that recorded with the esophageal electrode. Before supplemental doses of anesthesia were given, especially after vagotomy, the esophageal electrode, and in some cases the intramuscular electrodes, recorded phasic inspiratory activity not originating from the PCA. Therefore, one should be cautious in interpreting the activity recorded from esophageal electrodes as originating from the PCA, especially in conditions associated with increased respiratory efforts.


1985 ◽  
Vol 50 (1) ◽  
pp. 54-59 ◽  
Author(s):  
Thomas Shipp ◽  
Krzysztof Izdebski ◽  
Charles Reed ◽  
Philip Morrissey

EMG activity from four intrinsic laryngeal muscles (thyroarytenoid, posterior cricoarytenoid, interarytenoid, and cricothyroid) was obtained from one female spastic dysphonia patient while she performed a variety of speech and nonspeech tasks. These tasks were performed before and during a period of temporary unilateral laryngeal muscle paralysis. In the nonparalyzed condition, adductory muscle activity showed intermittent sudden increases that coincided with momentary voice arrests. These muscle patterns and accompanying voice interruptions were not present either when speech was produced in falsetto register or at anytime during the paralysis condition. The data suggest that individuals with this type of spastic dysphonia have normal morphology of recurrent laryngeal nerves and intrinsic laryngeal muscles, which means that the triggering mechanism(s) for spastic dysphonia symptoms must be located at some point neurologically upstream from the larynx.


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)


1993 ◽  
Vol 75 (3) ◽  
pp. 1088-1096 ◽  
Author(s):  
S. T. Kuna ◽  
M. P. McCarthy ◽  
J. S. Smickley

Passively induced hypocapnia in animals activates vocal cord adductor muscles and decreases the glottic aperture. The purpose of this study was to determine if passively induced hypocapnia has similar effects in normal adult humans in stage 3/4 non-rapid-eye-movement (NREM) sleep. Hypocapnia was induced by hyperventilating the subjects with a positive-pressure ventilator via a nose mask. At hypocapnic levels below the CO2 apneic threshold, abrupt cessation of mechanical ventilation was followed by an apnea. In protocol 1, intramuscular electromyographic recordings of intrinsic laryngeal muscles were obtained in nine subjects. Activity of the posterior cricoarytenoid muscle, a vocal cord abductor, disappeared during passive hyperventilation. The muscle remained electrically silent during an apnea, but phasic inspiratory activity reappeared with the first respiratory effort. The thyroarytenoid and arytenoideus muscles, both vocal cord adductors, were electrically silent during spontaneous breathing in NREM sleep. Hypocapnia was frequently associated with activation of both adductor muscles. Once activated, the adductor muscles remained tonically active during an ensuring apnea. In protocol 2, a fiber-optic scope was advanced transnasally into the hypopharynx to determine glottic aperture size during passively induced hypocapnic apnea. In the seven subjects who achieved stable NREM sleep, the glottic aperture during an apnea was smaller than at any time throughout the respiratory cycle during spontaneous breathing just before positive-pressure ventilation. The results suggest that the decrease in glottic aperture observed during an induced hypocapnic apnea is due to suppression of the posterior cricoarytenoid muscle and/or activation of vocal cord adductor muscles.


1990 ◽  
Vol 68 (4) ◽  
pp. 1746-1754 ◽  
Author(s):  
S. T. Kuna ◽  
J. S. Smickley ◽  
G. Insalaco

Six normal adults were studied 1) to compare respiratory-related posterior cricoarytenoid (PCA) muscle activity during wakefulness and sleep and 2) to determine the effect of upper airway occlusions during non-rapid-eye-movement (NREM) sleep on PCA activity. A new electromyographic technique was developed to implant hooked-wire electrodes into the PCA by using a nasopharyngoscope. A previously described technique was used to induce upper airway occlusions during NREM sleep (Kuna and Smickley, J. Appl. Physiol. 64: 347-353, 1988). The PCA exhibited phasic inspiratory activity during quiet breathing in wakefulness and sleep in all subjects. Discounting changes in tonic activity, peak amplitude of PCA inspiratory activity during stage 3-4 NREM sleep decreased to 77% of its value in wakefulness. Tonic activity throughout the respiratory cycle was present in all subjects during wakefulness but was absent during state 3-4 NREM sleep. In this sleep stage, PCA phasic activity abruptly terminated near the end of inspiration. During nasal airway occlusions in NREM sleep, PCA phasic activity did not increase significantly during the first or second occluded effort. The results, in combination with recent findings for vocal cord adductors in awake and sleeping adults, suggest that vocal cord position during quiet breathing in wakefulness is actively controlled by simultaneously acting antagonistic intrinsic laryngeal muscles. In contrast, the return of the vocal cords toward the midline during expiration in stage 3-4 NREM sleep appears to be a passive phenomenon.


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.


1993 ◽  
Vol 102 (2) ◽  
pp. 81-84 ◽  
Author(s):  
Roger L. Crumley

A review of our recent experience in patients with bilateral laryngeal paralysis is described. While we continue to use phrenic nerve transfers in patients with mobile arytenoids, patients with fixed arytenoids generally require some sort of vocal cord lateralization, either by arytenoidectomy and arytenoidopexy or by partial vocal cord resection. The endoscopic laser medial arytenoidectomy is a convenient and effective method for opening the posterior glottic airway. One arytenoid is reduced medially with the carbon dioxide laser. After about 3 months the opposite arytenoid can be treated similarly, if necessary. The procedure does not appear to affect arytenoid mobility, as the posterior commissure mucosa and underlying interarytenoid muscle are protected and hence unaffected by the procedure. Those patients with at least one mobile arytenoid cartilage are candidates for posterior cricoarytenoid muscle reinnervation. Although ansa cervicalis and phrenic nerve techniques have been described, the author has concentrated efforts on the phrenic nerve. This report describes the endoscopic laser medial arytenoidectomy procedure, while the phrenic nerve patients will be reported in a subsequent manuscript.


1994 ◽  
Vol 76 (3) ◽  
pp. 1262-1268 ◽  
Author(s):  
I. Kianicka ◽  
J. F. Leroux ◽  
J. P. Praud

In this study, we examined whether the glottis is open or closed during central apnea and the effect of arterial PO2 (PaO2) on this control. We hyperventilated nine 11- to 30-day-old awake nonsedated lambs via a tracheostomy for 1 min to induce central apnea. Four gas mixtures (8, 15, 21, and 30% O2) were used. At the end of the hyperventilation period, the lambs were allowed to breathe spontaneously through intact upper airways. Using a pneumotachograph attached to a face mask, we measured airflow, and we continuously recorded electromyographic (EMG) activity of the thyroarytenoid (TA), the main glottic adductor muscle. We also studied the lateral cricoarytenoid muscle (LCA, laryngeal adductor), the posterior cricoarytenoid muscle (PCA, laryngeal abductor), the cricothyroid muscle (CT), and the diaphragm. We found that hyperventilation consistently induced hypocapnic central apnea in all nine lambs in hyperoxic conditions [30% inspiratory fraction of O2 (FIO2)], in eight of nine lambs in normoxia or mild hypoxia (15 and 21% FIO2), and in four of seven lambs in hypoxia (8% FIO2). During baseline room air breathing, there was no glottic adductor muscle expiratory EMG activity or expiratory airflow braking. Continuous TA EMG activity began early during hyperventilation and continued throughout the central apnea, regardless of PaO2. The first subsequent breathing efforts were marked by expiratory flow braking and expiratory activity of the TA. The LCA and the TA demonstrated the same EMG activity pattern.(ABSTRACT TRUNCATED AT 250 WORDS)


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