Stimulation Of Superior Laryngeal Nerve Research Articles

Function of the Interarytenoid Muscle in a Canine Laryngeal Model

The interarytenoid (IA) muscle has rarely been studied in the living larynx. In this work, the role of the IA muscle in phonation was studied in three dogs by means of an in vivo phonation model. The isolated action of the IA muscle was studied by sectioning and stimulating its nerve branch. As IA activity increased, subglottic pressure increased significantly until a plateau was reached. In the absence of superior laryngeal nerve stimulation, the fundamental frequency rose with increasing IA activity. In the presence of superior laryngeal nerve stimulation, however, no significant change in fundamental frequency was observed with increasing IA activity. Measurement of adductory force demonstrated that the IA muscle adducts primarily the posterior vocal fold. In this canine model, phonation was not possible without IA stimulation, owing to a large posterior glottic chink.

Effects of RLN and SLN stimulation on glottal area.

In vivo canine experiments have demonstrated that vocal fold stiffness varies proportionately with changing levels of recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) stimulation. This study evaluated the morphologic changes in the glottis at varying levels of nerve stimulation and the presumed effects on laryngeal air particle velocity. Stroboscopic data from the in vivo canine model of phonation were examined under varying conditions of RLN and SLN stimulation. Computerized analysis of stroboscopic images was used to reconstruct the glottal area vs. time waveforms. As RLN stimulation increased, glottal area per cycle decreased (p < 0.05). However, as SLN stimulation increased, glottal area per cycle increased (p < 0.05). However, as SLN stimulation increased, glottal area per cycle increased (p < 0.05). These results support the hypothesis that increasing RLN stimulation at similar levels of SLN stimulation produces an increase in air particle velocity, whereas an increase in SLN stimulation causes a decrease in air particle velocity.

Nucleus tractus solitarius and excitatory amino acids in afferent-evoked inspiratory termination

This study tested the hypothesis that excitatory amino acid (EAA) neurotransmission at non-N-methyl-D-aspartate (non-NMDA), but not NMDA, receptors within medial regions of the nucleus tractus solitarius (NTS) is required in the inspiratory termination elicited by vagal or intercostal nerve (ICN) stimulation. Adult cats were anesthetized, decerebrated, vagotomized, and ventilated. After control responses to stimulation of the superior laryngeal nerve (SLN), vagus, and ICN were obtained, EAA receptor antagonists were injected into the medial aspects of the NTS. Injections of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 6,7-dinitro-quinoxaline-2,3-dione (DNQX), EAA receptor antagonists; (+/-)-2-amino-5-phosphonopentanoic acid (AP5), an NMDA antagonist; or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), a non-NMDA antagonist, ipsilateral to the vagus abolished the termination response. The SLN-elicited response persisted after AP5 injection but was abolished by NBQX injections. The ICN-elicited response persisted after bilateral injections of CNQX/DNQX or procaine. We conclude that the inspiratory termination elicited by ICN stimulation is independent of the regions medial to the NTS. Inspiratory termination elicited by vagal or SLN stimulation requires non-NMDA-mediated EAA neurotransmission within medial aspects of the NTS, but the vagally elicited response also requires NMDA receptors.

Central chemosensitivity affects respiratory muscle responses to laryngeal stimulation in the piglet

Stimulation of laryngeal afferent fibers triggers reflex apnea, which can be very long in the neonatal period. The purpose of this study was twofold: 1) to determine the effect of superior laryngeal nerve (SLN) stimulation on expiratory as well as inspiratory muscle activity and 2) to compare the respiratory response to SLN stimulation under conditions that would appear to alter the level of central chemosensitivity in anesthetized spontaneously breathing piglets. In protocol 1, we measured electromyogram (EMG) responses from the diaphragm (DIA), triangularis sterni, and transversus abdominis muscles to graded SLN stimulation; in protocol 2, we compared the DIA response to different levels of SLN stimulation during normocapnia, hypercapnia, and cooling of the ventrolateral medullary surface (VMS). SLN stimulation performed during normocapnia caused significantly greater inhibition of both expiratory muscles (triangularis sterni and transversus abdominis) than of the DIA. During hypercapnia, laryngeal stimulation-induced inhibition of all three muscles was significantly diminished, and the degree of inhibition for the three muscles became equivalent. Inhibition of the DIA EMG was significantly greater with SLN stimulation during VMS cooling than with a VMS temperature of 38 degrees C. We conclude that the magnitude of respiratory inhibition induced by laryngeal stimulation during early postnatal life is inversely related to the level of central chemical input and speculate that functional deficiency of structures located in the VMS may contribute to potentially life-threatening apnea in infants.

Effects of respiratory afferent stimulation on phrenic neurogram during hypoxic gasping in the cat.

Previous studies suggested that phrenic motor output is largely refractory to afferent stimuli during gasping. We tested this concept by electrically stimulating the carotid sinus nerve (CSN) or the superior laryngeal nerve (SLN) of anesthetized peripherally chemodenervated vagotomized ventilated cats during eupnea or gasping induced by hypoxia. During eupnea, phrenic neurogram amplitude (PNA) increased by 110% during 30 s of supramaximal CSN stimulation, but burst frequency did not change. Progressive hypoxia caused gasping after arterial O2 content was reduced by 75%. During gasping, CSN stimulation caused premature onset of gasp in 12 of 13 trials, shortened intergasp interval [6.3 +/- 0.9 vs. 14.8 +/- 2.5 (SE) s], and resulted in a small (20%) but significant increase in PNA. Intensity of SLN stimulation was adjusted to abolish phrenic activity during the 30-s eupneic stimulation period. During gasping, SLN stimulation of the same intensity tended to delay onset of the next gasp, increased intergasp interval (16.9 +/- 1.9 vs. 13.3 +/- 1.2 s), and reduced PNA by 32%. Thus the respiratory burst pattern formation circuitry responds to afferent stimuli during gasping, albeit in a manner different from the eupneic response. These observations suggest that gasping is the output of a modified eupneic burst pattern formation circuit.

Effect of tension, stiffness, and airflow on laryngeal resistance in the in vivo canine model.

This study used an in vivo canine model of phonation to determine the effects of airflow on glottal resistance at low, medium, and high levels of recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) stimulation. Static and dynamic trials of changing airflow were used to study the effects of airflow on glottal resistance during phonation. As reported previously, glottal resistance varies inversely as a function of airflow. Increasing levels of RLN stimulation resulted in a statistically significant increase in glottal resistance for each level of airflow evaluated. Variation in SLN stimulation had no statistically effects on the relationship between flow and resistance. At airflow rates greater than 590 milliliters per second (mL/s), glottal resistance approached 0.1 mm Hg per mL/s for all levels of RLN and SLN stimulation tested. These data support the collapsible tube model of phonation.

Determination of vocal fold mucosal wave velocity in an in vivo canine model.

The vocal fold traveling wave is essential to normal voice production. The present investigation examined whether the velocity of the traveling wave (TWV) could be consistently determined in an in vivo canine model and if traveling wave velocity is affected by changes in the amplitude of recurrent laryngeal nerve stimulation (RLNS) and superior laryngeal nerve stimulation (SLNS). The results showed that traveling wave velocity increased with an increase in recurrent laryngeal nerve stimulation at low constant superior laryngeal nerve stimulation, but was poorly correlated with increases in recurrent laryngeal nerve stimulation at a high level of superior laryngeal nerve stimulation. Furthermore, traveling wave velocity was significantly correlated with superior laryngeal nerve stimulation at constant recurrent laryngeal nerve stimulation. This study demonstrated the feasibility of objectively measuring traveling wave velocity in vivo.

Laryngeal resistance of an in vivo canine model of phonation with a constant air pressure source

Previous studies of laryngeal biomechanics using in vivo models have generally used a constant air flow source. Several authors have recently suggested that during phonation, the lung–thorax system functions as a constant pressure source. The present paper describes an in vivo canine system designed to maintain a constant peak subglottic pressure (Psub) using a pressure‐controlling mechanism. It was found that with a decrease in Psub, the range of recurrent laryngeal nerve stimulation (RLNS) voltage needed to induce phonation was reduced. At a given superior laryngeal nerve stimulation (SLNS) level and Psub, increasing levels of RLNS resulted in a normal distribution of vocal efficiencies. For each SLNS and Psub, minimum and maximum levels of RLNS were determined outside of which no phonation was possible. Levels of RLNS that produced an optimal stable phonation were also identified. Increasing levels of RLNS resulted in significant decreases in glottal air flow. Contrary to a previous report using a constant flow source, increasing levels of SLNS produced a significant decrease in glottal resistance. This is consistent with another previous study [D. M. Moore and G. S. Berke, J. Acoust. Soc. Am. 83, 705–714 (1988)] demonstrating that the open quotient increased with increasing SLNS.

Interaction between central pattern generators for breathing and swallowing in the cat.

1. We examined the interaction between central pattern generators for respiration and deglutition in decerebrate, vagotomized, paralysed and ventilated cats (n = 10), by recording activity from the following nerves: hypoglossal, phrenic, thyroarytenoid and triangularis sterni. Fictive breathing was spontaneous with carbon dioxide above the apnoeic threshold (end-tidal PCO2, 32 +/- 4 mmHg) and fictive swallowing was induced by stimulating the internal branch of the left superior laryngeal nerve (SLN) continuously (0.2 ms pulse duration, 10 Hz). 2. In all ten animals, SLN stimulation evoked short bursts of thyroarytenoid and hypoglossal nerve activity indicative of fictive swallowing. In two of ten animals, respiration was inhibited completely during deglutition. In the other eight animals, fictive breathing and swallowing occurred simultaneously. 3. With SLN stimulation below threshold for eliciting swallowing, the respiratory rhythm decreased, the duration of inspiration did not change but the duration of expiration, especially stage II, increased. Integrated nerve activities indicated that the rate of rise and peak of phrenic nerve activity decreased, stage I expiratory activity of the thyroarytenoid and especially that of the hypoglossal nerve increased and stage II expiratory activity of the triangularis sterni nerve was suppressed completely. However, if inspired carbon dioxide was increased, i.e. hypercapnic ventilation, stage II expiratory activity remained partially during continuous SLN stimulation. 4. Fictive-swallowing bursts occurred only at respiratory phase transitions. At the minimal stimulus intensity that evoked repetitive swallowing bursts, the pattern of interaction between breathing and swallowing central pattern generators was consistent for each animal (n = 7) but was different across animals. In four animals, fictive swallows occurred at the phase transition between stage II expiration and inspiration, at the transition between inspiration and stage I expiration in one animal; and in two other animals, at the transition between stage I and II of expiration. 5. The response to SLN stimulation accommodated during the stimulus train. Accommodation was evident in both the interswallow interval (ISI) which lengthened, and the interaction pattern which had fewer swallows per breath as the stimulus period progressed. In contrast to the ISI, characteristics of the fictive swallow did not accommodate. For example, duration of the swallow was constant, distributed over a narrow range throughout the stimulus train. 6. We conclude that the central pattern generators for swallowing and breathing interact. The pattern of interaction supports the three-phase theory of respiratory pattern generation.(ABSTRACT TRUNCATED AT 400 WORDS)

Excitatory amino acid neurotransmission in superior laryngeal nerve-evoked inspiratory termination.

Superior laryngeal nerve (SLN) stimulation elicits a transient inhibition of inspiration (single shocks) or inspiratory termination (stimulus trains). The neural pathways mediating these responses are unknown, but the medial nucleus tractus solitarius (mNTS) has been implicated in the termination reflex. This study tested the hypothesis that SLN-evoked inspiratory termination requires excitatory amino acid (EAA) neurotransmission in medial aspects of the NTS. Experiments were conducted in decerebrate, vagotomized, and paralyzed adult cats. Inspiratory motor output was recorded from the phrenic nerve. After control responses to SLN stimulation were recorded, a unilateral injection of the EAA antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 10 mM) was made into the mNTS. The transient inhibitions were not altered by DNQX. Inspiratory termination elicited by stimulation of the SLN contralateral to the injection persisted after DNQX (n = 4). Stimulation of the ipsilateral SLN no longer elicited termination (5 of 9 animals) or did so only at greatly elevated thresholds (4 of 9). We conclude that EAA neurotransmission in the mNTS is not required in the transient reflex but is necessary for the production of the SLN-evoked inspiratory termination.

Phase-dependent dynamic responses of respiratory motor activities following perturbation of the cycle in the cat.

1. Electroneurographical (ENG) activities of a phrenic nerve, a thyroarytenoid (TA) branch of a recurrent laryngeal nerve, and a triangularis sterni (TS) branch of an internal intercostal nerve were recorded in decerebrate, vagotomized and paralysed cats. A superior laryngeal nerve (SLN) was stimulated electrically. Our objective was to evaluate transient changes in motor activity following a brief perturbation of the respiratory cycle by SLN stimulation. 2. Each motor nerve recorded represents a separate phase of the respiratory cycle. We measured the duration of phrenic ENG activity for inspiratory phase duration (TI) and similarly the duration of TA and TS ENG activity for the duration of stages I and II of expiration, respectively. Changes in the duration of the total respiratory cycle (TTOT) were also measured. Therefore, the changes in TTOT were accounted for directly by changes in each phase of the respiratory cycle. 3. Perturbation during the inspiratory phase inhibited phrenic activity either reversibly or irreversibly (premature termination of inspiration) depending on the strength and timing of the stimulus. Reversible inhibition of inspiration was associated with a transient activation (< 100 ms) of the TA nerve followed by a reactivation of the phrenic nerve, but the duration of the subsequent stages I and II of expiration remained the same. Thus, the prolongation of TTOT was completely accounted for by the lengthening of TI. 4. Premature termination of inspiration was followed by either a shortening (the first half of inspiration) or a lengthening (the second half of inspiration) of the duration of stage I expiration and consistently by a shortening of the duration of stage II expiration. The magnitude of these changes in the durations of stages I and II of expiration was phase dependent. Changes in the duration of all three phases of motor activity contributed to the changes in TTOT. 5. Perturbation during stage I expiration prolonged this stage but did not affect the duration of the succeeding stage (stage II expiration). The increase in the duration of stage I expiration appeared constant and not dependent on the time when the perturbation was delivered in stage I expiration. Thus, the change in TTOT was less phase dependent during stage I expiration than during inspiration and stage II expiration and was accounted for by changes in the duration of TA activity alone. 6. Perturbation during stage II expiration inhibited TS activity and evoked TA activity transiently.(ABSTRACT TRUNCATED AT 400 WORDS)

Laryngeal brain stem evoked response in the porcine model.

Exaggeration of normally protective laryngeal reflexes is thought to play a role in several disorders, including the sudden infant death syndrome. An analysis of brain stem neural activity following laryngeal stimulation may provide insight into the pathophysiology of pathologic laryngeal reflexes and help to identify individuals at risk for these disorders. The purpose of this study was to define the far-field brain stem activity following laryngeal stimulation in the porcine model. This activity has been termed the laryngeal brain stem evoked response and may represent a potentially useful and objective measure of the neuronal activity in the laryngeal reflex pathway. Electrical stimulation of the superior laryngeal nerve was performed in 14 mixed-breed piglets under a variety of physiologic conditions. A total of six positive and six negative discrete waves were detected, with mean latencies ranging from 1.24 to 7.16 milliseconds. Stimulations performed during hypoxic, hypercapneic, or hypocapneic conditions resulted in no significant differences in waveform latencies. There appears to be a reproducible, but somewhat variable, brain stem response elicited by superior laryngeal nerve stimulation that can be recorded via a far-field technique in the porcine model.

Actions of carotid chemoreceptors on subretrofacial bulbospinal neurons in the cat

Thirty-one barosensitive bulbospinal neurons were recorded from the subretrofacial (SRF) nucleus in eight chloralose-anaesthetised, paralysed cats. Close arterial injections of CO 2-saturated saline were used to stimulate carotid body chemoreceptors. Seven neurons were abruptly excited and six neurons abruptly inhibited by chemoreceptor stimuli: these were primary responses, independent of changes in blood pressure or central respiratory drive (monitored from the phrenic nerve). A further eight neurons responded only indirectly to chemoreceptor stimuli, showing enhanced modulation of their activity coupled to the enhanced central respiratory drive. The distinction between primary and secondary responses was shown more clearly when central respiratory drive was inhibited by superior laryngeal nerve stimulation. The remaining ten neurons showed no clear response to chemoreceptor stimuli. SRF bulbospinal neurons thus show the same range of responses to chemoreceptor stimuli as the sympathetic neurons they are believed to drive.

Entrainment of respiratory rhythm to respiratory oscillations of arterial PCO2 in vagotomized dogs.

The aim of this study was to demonstrate that the medullary respiratory rhythm generator is capable of entraining to respiratory oscillations of arterial PCO2 (CO2 oscillations). We used 10 anesthetized, paralyzed, vagotomized, and mechanically ventilated dogs. First, rate of mechanical ventilation was manually adjusted so that it matched the dog's spontaneous respiratory rate, which established a constant phase relationship between the mechanical ventilation and the burst of phrenic neurogram (initial phase). Then this phase relationship was temporally disturbed by a brief electrical stimulation of the superior laryngeal nerve (SLN). In the control group, the initial phase and the steady-state phase relationship after SLN stimulation were randomly distributed within the phase plane, implying no interaction between the respiratory center and mechanical ventilation. In contrast, when CO2 output from the lung was increased 2.6-fold above the control level by venous CO2 loading, the initial phase and the steady-state phase after SLN stimulation were locked in such a way that the onset of the burst of phrenic neurogram coincided with the peak of CO2 oscillations. This was not demonstrated when the dog was made hyperoxic. We therefore conclude that the respiratory center could entrain to phasic chemical afferent inputs originating from CO2 oscillations, provided they are considerably amplified.

Effects of cricothyroid muscle contraction on upper airway flow dynamics in dogs.

We studied the effects of cricothyroid muscle (CT) contraction on upper airway flow dynamics in eight prone open-mouth anesthetized dogs. Animals were mechanically ventilated via a tracheostomy while a constant airflow (Vuaw) passed through the isolated upper airway. Nasal airflow (Vn) was monitored using a nasal mask and pneumotachograph. Bilateral CT contraction was induced by electrical stimulation of the external branches of the superior laryngeal nerves. During CT contraction with Vuaw of 100-443 ml/s in the inspiratory direction, total upper airway resistance (Ruaw) fell by 49.1 +/- 5.4% (SE) while supraglottic resistance fell by 63.6 +/- 3.6%; simultaneously Vn fell by 55.3 +/- 3.8% and Vuaw increased by 7.2 +/- 1.7%. Similar results were obtained when Vuaw was in the expiratory direction. In three dogs in which the attachments of the CT to either the thyroid or cricoid cartilage were severed, superior laryngeal nerve stimulation had no systematic effect on Ruaw. Because visual assessment during CT contraction consistently revealed dilation of the piriform recesses, we suggest that CT contraction is associated with pharyngeal dilation, which in open-mouth dogs (with overlapping soft palate and epiglottis) redistributes flow to the oral route with a net reduction in Ruaw. Thus the CT may have a respiratory role as a pharyngeal dilator.

Morphology and electrophysiology of superior laryngeal nerve afferents and postsynaptic neurons in the medulla oblongata of the cat

Intra-axonal recordings were made from 24 afferent fibres of the superior laryngeal nerve in and around the nucleus tractus solitarius, in 26 pentobarbitone-anaesthetized cats. Conduction velocity ranged from 15 to 38 m/s. Four afferents were injected with horseradish peroxidase. They showed dense terminal arborization in the region of the ventral and ventrolateral subnuclei of the nucleus tractus solitarius, both rostral and caudal to the obex. Six other intra-axonal recordings were thought to originate from axons of neurons postsynaptic to superior laryngeal afferents; one of these was injected with horseradish peroxidase and showed a similar arborization pattern to that of the afferent axons. In the same region, intracellular recordings were made from 124 neurons which responded to superior laryngeal nerve stimulation with excitatory postsynaptic potentials (mean latency 2.7 ± 1.0 ms). Ninetynine of these neurons were thought to receive a monosynaptic input. The stimulation threshold evoking-these responses was similar to that which inhibited phrenic nerve discharge. Eleven of the monosynaptically excited neurons were injected with horseradish peroxidase. They had fusiform or stellate somata and simple dendritic trees, radiating mainly in the transverse plane. In one experiment, in which both a superior laryngeal nerve afferent fibre and a neuron were labelled, afferent terminal varicosities were found in close apposition with the postsynaptic membrane of the injected neuron. Four of 14 (29%) tested neurons could be antidromically activated from the C 3 spinal segment. The stimulus thresholds and onset latencies of the responses of superior laryngeal nerve afferents and medullary neurons to stimulation of the superior laryngeal nerve are consistent with their involvement in the reflex inhibition of respiratory neurons evoked by superior laryngeal nerve stimulation.

Effects of intravenous bicuculline and strychnine on inspiratory inhibitory responses in the cat

Single shock stimulation of the superior laryngeal nerve (SLN), intercostal nerve (ICN), phrenic nerve (PN) or within the medullary respiratory groups (DRG-VRG) produces a transient, short-latency attenuation of inspiratory motor activity. Trains of stimuli delivered to SLN and ICN cause premature termination of inspiration. This study examined involvement of glycine and GABA A receptors in these reflex inhibitions. Experiments were conducted in decerebrate, vagotomized, and paralyzed cats. Control responses of left PN activity to threshold single shock stimulation of SLN, PN, ICN and the DRG-VRG were recorded and the thresholds for SLN- and ICN-evoked inspiratory termination were determined. Five min after intravenous injection of bicuculline (1 mg/kg) or strychnine (50 μg/kg), the responses to stimulation were again recorded. This procedure was reiterated until the cumulative dose elicited marked convulsions. Neither drug affected the inspiratory terminating reflexes. Systemic bicuculline had no effect on transient inspiratory inhibition. However strychnine prolonged the onset latency and the duration of all four inhibitory responses. Since the degree of transient inhibition was not lessened (only delayed), it appears that these inspiratory inhibitory reflexes do not rely exclusively on actions of glycine or GABA A receptors.

Synaptic interaction between medullary respiratory neurones during apneusis induced by NMDA-receptor blockade in cat.

1. Termination of inspiration is an essential component of respiratory rhythm generation and its perturbation can result in apneusis, i.e. significant prolongation of mechanisms, we studied the postsynaptic events in respiratory neurones during apneustic respiratory periods, and compared them to normal respiratory cycles. 2. Experiments were performed in pentobarbitone-anaesthetized, paralysed, thoracotomized cats ventilated with a constant volume or a cycle-triggered constant pressure pump. Apneusis, separated by normal cycles, was induced as follows: the animal was ventilated by a cycle-triggered pump that normally inflated the lungs during the inspiratory burst of phrenic nerve discharge. The NMDA-receptor blocker MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5, 10-iminemaleate] (0.3-0.7 mg/kg) was administered intravenously, and, for designated breaths, inflation of the lungs was withheld during neural inspiration. 3. Membrane potential trajectories of forty-one late expiratory (E-2) and eight postinspiratory (PI) neurones of the caudal ventral respiratory group were analysed before and/or after MK-801 administration, during normal and apneustic periods. 4. Before MK-801 administration, withholding lung inflation caused modest (10-20%) lengthening of the inspiratory period; after MK-801 administration, withholding inflation caused apneusis. Provided that the lungs were inflated during the inspiratory phase, the temporal pattern of phrenic nerve, recurrent laryngeal nerve and membrane potential trajectories of E-2 and PI neurones were not significantly altered by MK-801. Apneusis following NMDA-receptor blockade produced consistent changes in the synaptic activation patterns of E-2 neurones. In particular, the slow late inspiratory-related depolarization pattern of E-2 neurones was consistently retarded during apneustic inspiratory phases when compared to normal inspiratory phases. This was due to continuation of Cl(-)-mediated synaptic inhibition of E-2 neurones. Superior laryngeal nerve stimulation stopped apneusis and sustained membrane hyperpolarization of E-2 neurones similar to lung inflation. 5. During the plateau phase of apneusis, correlated 10-20 Hz oscillations could be observed in the integrated phrenic and recurrent laryngeal nerve activities as well as in the membrane potential of E-2 neurones. 6. We conclude that: (i) the prolonged inhibition of E-2 neurones during apneusis is indicative of the process responsible for the prolongation of the inspiratory phase.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of RLN and SLN stimulation on glottic area.

In vivo canine experiments have demonstrated that vocal fold stiffness varies proportionately with changing levels of recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) stimulation. This study evaluates the morphologic changes in the glottis at varying levels of nerve stimulation and the effects on laryngeal resistance. Stroboscopic data from the invivo canine model were examined under varying conditions of RLN and SLN stimulation. Computerized analysis of stroboscopic images was used to reconstruct the glottic area versus time waveforms and the results will be presented. Glottal dynamics were measured using photoglottography, electroglottography, and the glottal area waveforms. The effects of varying RLN and SLN stimulation on laryngeal resistance will be discussed. [Work supported by an American Laryngologic Research Award.]

Antagonistic interaction of laryngeal and central chemoreceptor respiratory reflexes.

Stimulation of laryngeal afferent fibers evokes a profound reflex inhibition of central respiratory drive. The interaction of this airway reflex with chemoreceptive ventilatory control mechanisms is poorly understood. The present study was undertaken to determine whether there is significant interaction between the effects of central chemoreceptor and laryngeal afferent stimulation on central inspiratory activity and, if so, to also determine the nature of the interaction. The effect of electrical stimulation of the superior laryngeal nerve (SLN) on the timing and intensity of central inspiratory activity was determined from the rectified and filtered phrenic neurogram in 10 dogs. Each dogs was decerebrated, artificially ventilated, vagotomized, and had the carotid bodies denervated. In each case, stimulation of the right SLN at 3 and 10 Hz caused a frequency-dependent slowing or arrest of central inspiratory activity. Increases in arterial PCO2 (PaCO2) attenuated the absolute level of inhibition of central inspiratory activity recorded during both SLN stimulation and control periods. Tp clarify the nature of the interaction between chemoreceptor and laryngeal afferent stimulation, the relationship between PaCO2 and central inspiratory activity was investigated during stimulation of the SLN at 0, 3, and 10 Hz. Control central inspiratory activity increased as a sigmoidal function of PaCO2. This sigmoidal relationship was greatly depressed during SLN stimulation but did not appear to be shifted along the PaCO2 axis. The results of this study therefore suggest that the interaction between central chemoreceptor and laryngeal afferent stimulation is multiplicative: the inhibition of the central inspiratory activity is mediated by an attenuation and not a resetting of central chemoreflexes.