Laryngeal Stimulation Research Articles

Jet ventilation for laser laryngeal surgery in children. Modification of the saunders jet ventilation technique

In our clinical series, 40–50% O 2 and 50–60% N 2O (regulated by a blender and delivered by manual jet ventilation (MJV)) and residual halothane from induction provided satisfactory supralaryngeal anesthesia. Fentanyl, N 2O, atracurium, and lidocaine administered i.v. effectively blunted laryngeal stimulation, allowed control of respiration, and minimized vocal cord motion. Wide unobstructed surgical access to the entire endolarynx is provided. Atracurium (an intermediate-acting non-depolarizing muscle relaxant administered in a single bolus or by constant infusion) achieves the needed level of blockade and permits the anesthesiologist to focus on the pattern of respiration rather than the degree of neuromuscular blockade. Its duration of action seems to be well matched to the average duration of this surgical procedure. Because its reversal is prompt (35–45 min from i.v. injection to 25% recovery by neuromuscular transmission monitor) (Brandom et al, Clinical pharmacology of atracurium in paediatric patients, Br. J. Anaesth., 55 (1983) 117S–121S) children can be discharged safely from the recovery room to home after an appropriate period of observation in the short-stay unit. Our report confirms and extends another recent report supporting supraglottic jet ventilation (Scamman, F.L. and McCabe, B.F., Supraglottic jet ventilation for laser surgery of the larynx in children, Ann. Otol. Rhinol. Laryngol., 95(1986) 142–145). We belive that the MJV techinique is advantageous in children, particularly for outpatient surgery. Attention to detail and careful communication between a skilled anesthesilogist and surgeon are essential. Dangerous barotrauma can occur and skill and monitoring are essential.

Reflex decrease of histamine-induced bronchoconstriction after laryngeal stimulation in humans.

The aim of this work was to determine whether the nonadrenergic, noncholinergic, inhibitory nervous system can be reflexly activated in humans by laryngeal stimulation. The stimulation was achieved with a cytology brush passed through a bronchoscope previously introduced transnasally and positioned just above the epiglottis. In one series of experiments, subjects were premedicated with beta-adrenergic and cholinergic blockers, and bronchoconstriction was induced by histamine inhalation. The results showed that mechanical irritation of the vocal cords with the cytology brush produced a sharp, short-lasting (less than 1 min) decrease in RL from (mean +/- SE) 6.8 +/- 2.1 to 4.8 +/- 1.5 cm H2O.L-1.s, and in the absence of parasympathetic blockade, laryngeal irritation produced a fall in RL from (mean +/- SE) 9.0 +/- 3.7 to 5.4 +/- 2.0 cm H2O.L-1.s (p less than 0.0001) (ANOVA). This decrease in RL was independent of the slight cough produced by laryngeal stimulation and reflects a change in lower and not upper airway resistance. Adequacy of the beta-adrenergic and cholinergic blockade was checked with an intravenous infusion of isoproterenol and inhaled methacholine, respectively. In 2 subjects, the fall in RL was abolished by a block of the superior laryngeal nerves and direct local anesthesia of the vocal cords. We conclude that mechanical irritation of the larynx produces a partial reversal of histamine-induced bronchoconstriction that is mediated through nervous pathways that are neither beta-adrenergic nor cholinergic in origin. We suggest that this decrease in bronchoconstriction is modulated by the nonadrenergic, noncholinergic, inhibitory nervous system.

Effects of nasal and laryngeal stimulation upon peripheral lung function.

Arterial hypoxemia and sudden death have been associated with the placement of posterior packs for control of severe epistaxis. There exists some controversy as to the mechanism underlying the clinically observed hypoxemia; some authors postulate a nasal pulmonary reflex as the basis for the hypoxemia. In an attempt to further investigate this theory, collateral ventilation was measured in the dog model during nasal and laryngeal stimulation. Collateral ventilation is thought to be one of the most sensitive techniques available to assess the resistive and elastic properties of the lung periphery. In the dog, with respiratory rate controlled (i.e., anesthetized and paralyzed), nasal stimulation with mechanical, thermal, and chemical stimuli failed to affect collateral ventilation. This finding suggests that the reflex may be acting either in larger lung segments or on the pulmonary vascular bed itself.

Respiratory changes induced by prolonged laryngeal stimulation in awake piglets.

To examine the role of the laryngeal reflex in modulating cardiorespiratory function, we stimulated the superior laryngeal nerves (SLN) bilaterally in unanesthetized, chronically instrumented piglets (n = 10, age 5-14 days). The SLN were placed in cuff electrodes and wires were exteriorized in the neck for stimulation. A cannula placed in the aorta was used for blood pressure recording and arterial blood sampling. During each experiment, 1-2 days after surgery, ventilation was recorded using whole-body plethysmography, and electroencephalogram and electrocardiogram were recorded after acute subcutaneous electrode placement. After base-line recordings, the SLN were electrically stimulated for 1 h. During this period, mean respiratory frequency decreased by 40-75% and apneas of 10-15 s were regularly interspersed between single breaths or clusters of breaths. Periods of breathing were always associated with opening of the eyes and generally with head and body movements, an awakening that occurred every 10-15 s. At 1 h into the stimulus period, minute ventilation had decreased by 57 +/- 7% (mean +/- SE), arterial partial pressure of O2 (PaO2) by 68 +/- 3 Torr, and arterial partial pressure of CO2 (PaCO2) had increased by 19 +/- 2 Torr. Throughout the entire stimulus period, mean blood pressure and average heart rate were maintained within 12% of base line. We suggest that: low-threshold SLN afferents exert primarily respiratory effects and only minor cardiovascular effects; breathing during laryngeal reflex activation is sustained by an arousal system; and the laryngeal reflex does not pose an imminent threat to the unanesthetized, awake, young animal.

Reflex activation of the nonadrenergic noncholinergic inhibitory nervous system in feline airways.

Experiments were undertaken to learn if the nonadrenergic noncholinergic inhibitory nervous system (NANCIS) in feline airways could be activated reflexly either by mechanically stimulating the laryngeal mucosa or by inducing acute bronchospasm with boluses of 5-hydroxytryptamine (5HT) injected intravenously. Mechanical stimulation of the dorsal laryngeal mucosa evoked a biphasic bronchomotor response in anesthetized cats that had received intravenously an infusion of 5HT to raise their basal airway smooth muscle tone. The response consisted of a transient augmentation of bronchoconstriction followed by a prolonged bronchodilation. After muscarinic cholinergic receptor blockade with atropine, the constriction phase of the response disappeared, but the relaxation phase persisted. Bronchodilation elicited by laryngeal stimulation was resistant to beta-adrenergic receptor blockade with propranolol but was abolished by autonomic ganglionic blockade with hexamethonium and blocked reversibly by vagal cooling. The latter interventions, when imposed between successive dose-response curves generated by intravenous 5HT in animals pretreated with atropine and propranolol, did not alter the positions or slopes of the curves. These findings support the conclusion that mechanical stimulation of the larynx reflexly activates not only the well-known vagal cholinergic excitatory pathway to the airways but also the more recently described vagal, nonadrenergic noncholinergic inhibitory pathway. The results further indicate that bronchoconstriction is neither a prerequisite for the bronchodilator component of the laryngeal bronchomotor reflex nor an independent initiating stimulus for NANCIS-mediated reflex bronchodilation.

Ventilatory and waking responses to laryngeal stimulation in sleeping mature lambs

Ventilatory and waking responses to laryngeal stimulation were studied in six chronically tracheostomized lambs breathing through an endotracheal tube. A balloon catheter inserted in the rostral tracheal segment allowed application of distilled water onto the larynx. Apnea, the main primary ventilatory response, was shorter in wakefulness (7.9 sec) than in quiet (10.7 sec) or active sleep (10.6 sec, residual variance= 3.29), where the response to laryngeal stimulation was poorly reproducible. Arousal delay measured from the neck muscle EMG was longer in active (21.1 sec) than in quiet sleep (5.4 sec, residual variance= 9.05). Arousal preceded apnea termination more often in quiet than in active sleep. When breathing resumed a sigh frequently occurred following prolonged apneas. We conclude that laryngeal stimulation elicits apnea in all states in mature lambs. The termination of apnea is related to waking up in quiet but not in active sleep. where arousal is depressed. A comparison of our results with data from preterm and adult mammals strongly suggests that the ventilatory response to laryngeal stimulation during active sleep is unaffected by maturation.

Effect of alcohol on apnea reflexes in young lambs.

This study examined the effect of alcohol on two apnea reflexes considered to be protective mechanisms through which animals and humans preserve vital functions while they are submerged in water. The laryngeal chemoreflex and the trigeminal diving reflex were studied in unanesthetized 1- to 3-wk-old lambs. Reflex stimulation resulted in reduced ventilation or apnea, bradycardia, hypertension, and blood flow redistribution in the dive pattern. After alcohol, reflex stimulation resulted in increased apnea response, preserved blood flow redistribution, but less hypertension. The onset of regular breathing following laryngeal water stimulation was significantly delayed, after alcohol, and mechanical ventilation was used in three lambs to terminate the prolonged poststimulus apnea. Airway occlusion pressure, an index of neuromuscular inspiratory drive, decreased significantly after alcohol. The study demonstrates a potent effect of alcohol on apnea reflex responses. The effect of alcohol on respiratory drive and on the apnea reflex response should be considered when humans ingest alcohol, in particular by those participating in water sports.

The development of cough.

Control of coughing is immature at birth; less than half of newborns cough spontaneously or on direct laryngeal stimulation. It is not known whether timing and distribution of motor outflow is optimized for muscle and lung mechanics. The musculoskeletal system is immature. Inspiratory and expiratory pressures appear to be adequate at birth, but the ranges of pressures and volumes actually used by infants during coughing are not well known. Lung structure is immature at birth. Low lung recoil pressures and low tracheal elastance (easy collapsibility) probably combine to reduce maximal gas velocities in uncompressed intrathoracic airways, and relatively low maximal expiratory pressures and high flow-resistive losses may combine to reduce maximal velocities in compressed regions of intrathoracic airways. Better descriptions of normal and pathologic aspects of structure and function are needed, with attention to control, motor, and lung mechanical functions during coughing and forced expiration in human infants. Application to the developing respiratory system of scaling techniques and models of forced expiration, and advances in understanding of two-phase flow in airways, would be helpful.

Function of the larynx in the fetus and newborn.

The muscles of the larynx function as a part of the respiratory system before birth, and like other respiratory muscles, have experienced considerable use by the moment of birth. In late fetal life the larynx appears to influence the outward flow of pulmonary liquid and thus may play a role in lung development. Immediately after birth and in cases of neonatal lung disease, elevated pressures within the airways during expiration, probably a result of laryngeal adduction, are involved in the maintenance of FRC. This mechanism is also present, to a lesser degree, in normal ovine (and probably human) neonates during quiet sleep. Whether it exists in other species remains to be established. Expiratory resistance of the larynx is under vagal control, and pulmonary stretch receptors are the likely sensors. Species differences apparently exist in the means by which expiratory airflow is retarded. These may be due in part, however, to the widespread use of anesthetic agents that selectively depress the activity of laryngeal adductor muscles. There is clearly a need for wider use of techniques involving chronic instrumentation, particularly in the neonatal period. Because the upper airway is involved in the regulation of tidal airflow, it also seems vital that the airway remains intact wherever possible. In addition to controlling airflow, the larynx is an important sensory organ, protecting the lower airways from invasion by potentially harmful substances, e.g. during suckle feeding and regurgitation. In the neonate, laryngeal stimulation may result in prolonged respiratory arrest. Although there is some evidence that longer apnea can be elicited in the neonate than in the adult, the use of anesthesia, which may more strongly depress respiration in the young, complicates the issue. As yet, there are no firm grounds for explaining these findings, at either a peripheral or central level. Defensive mechanisms, including arousal, swallowing, and circulatory changes to cope with hypoxemia, are well established at birth. The healthy neonate would seem well equipped to survive entry of liquids into the larynx. However, it is not inconceivable that, under certain circumstances and in the absence of anesthesia, substances entering the larynx could trigger prolonged apnea or cardiac arrest.

New approaches to regulation of fluid secretion in airways.

Physiologic, morphologic, biochemical, and immunologic methods have been used to study cholinergic and adrenergic regulation of airway submucosal gland secretion. Using a newly developed micropipette method, we can now measure the rate of fluid flow from each individual gland duct and we can harvest these secretions for specific chemical analysis. Stimulation of both the cholinergic and adrenergic systems affect gland secretions. The vagus nerves are the pathways for many reflexes affecting secretion: laryngeal, gastric and carotid body chemoreceptor stimulation accelerate the fluid production, and lung inflation (Hering-Breuer reflex) inhibits fluid secretion. Stimulation by cholinergic, muscarinic agonists depletes both mucous and serous cells, so vagal reflexes probably produce mixed secretions. In contrast, alpha-adrenergic agonists deplete serous cell contents, release high concentrations of lysozyme and produce large volumes of fluid with a low protein concentration, while beta-adrenergic stimulation may selectively deplete mucous cells, releases little lysozyme and produces scanty fluid with a high protein concentration. The significance of this cholinergic and adrenergic modulation on cough and ciliary clearance are important subjects for future study.

Micropipette measurement of airway submucosal gland secretion: laryngeal reflex.

We used our microcollection technique to study the effect of mechanical stimulationof the larynx on tracheobrochial gland secretion. The basal secretory rate of 8 glands in 5 cats rose from 18.6 +/- 2.0 nl/min (mean +/- SE) to a maximum of 47.8 +/- 4.0 nl/min within 1 min of mechanical stimulationof the laryngeal mucosa(p < 0.005) and returned to prestimulation levels within 4 to 5 min after cessation of the stimulus. The effect of laryngeal stimulation on gland secretion was prevented by cooling both cerevical vagi to - 3 degrees C before and during stimulation, and was restored by warming both vagito 37 degrees C before stimulaltion. Atropine sulfate (0.5 mg/kg given intravaenously) also prevented the secretory response to laryngeal stimulation. Transsection of the sensory nerves to the larynx blocked this response as well. Electrical stimulation (7 V, 20 Hz, 15 s) of the central end of the cut superior layyngeal nerve increased the rate of secretion of 6 glands in 5 cats from 10.0 +/- 2.0 nl/min to 26.0 +/- 3.0 nl/min (p < 0.01); atropine also prevented this effect.

Effects of chemical drive on the inhibition of respiration produced by laryngeal stimulation in cats.

In 8 anesthetized cats the acute respiratory responses to laryngeal stimulation were studied under various levels of chemical drive. Under air breathing condition with strong stimulation the animals showed either cough or apnea, whereas with relatively weak stimulation the animals showed smooth reduction in respiration due to a decrease in tidal volume and prolongation of both inspiratory and expiratory time. Although the inhibitory effect of laryngeal stimulation on tidal volume was independent of the level of chemical drive, the inhibition of respiration, when analyzed in terms of decrease in the minute ventilation, was greater the higher the chemical drive regardless of the type of chemical stimulus. Although bilateral vagotomy decreased the threshold of stimulus intensity for changes in respiratory pattern, especially under hypoxia, the effects of laryngeal stimulation on respiratory pattern in vagotomized animals were qualitatively similar to those obtained in the intact animals. We concluded that laryngeal stimulation has a direct action on the central respiratory mechanism regulating respiratory duration and that the interaction between laryngeal stimulation and chemical drive causes multiplicative inhibitory effects on ventilation.

Waking and ventilatory responses to laryngeal stimulation in sleeping dogs

We studied waking and ventilatory responses to laryngeal stimulation during sleep in three dogs. The dogs breathed through an endotracheal tube inserted caudally into the trachea through a tracheostomy. Laryngeal stimulation was produced either by inflating a small balloon that was positioned in the rostral tracheal segment, or by squirting water onto the larynx through a catheter inserted through the tracheostomy. Airflow was measured with a pneumotachograph, and sleep state was determined by behavioral, electroencephalographic, and electromyographic criteria. We found that the degree of laryngeal stimulation required to produce arousal and coughing was higher in rapid-eye-movement (REM) sleep than in slow-wave sleep (SWS). Stimuli that failed to cause arousal from SWS often produced a single expiratory effort, or brief apnea (1--2 s) and bradycardia. In contrast, during REM sleep subarousal stimuli often resulted in prolonged apnea (greater than 10 s) and marked bradycardia. We conclude that during REM sleep arousal responses to laryngeal stimulation are depressed, but ventilatory and cardiac responses are intact.

Laryngeal reflex regulation: Peripheral and central neural analyses

Because of the many functions (e.g., glottic closure, gagging, coughing, swallowing, speech) in which the internal laryngeal muscles are active, complex regulatory mechanisms must exist to modify and coordinate these activities. Little information is available, however, on these neural mechanisms, and the present study attempted to provide more information by investigating, in the adult cat, the effects of stimuli to various orofacial and upper respiratory tract sites and nerves on 110 single units recorded in individual laryngeal muscles, in the recurrent laryngeal nerve (RLN), and in the brain stem nucleus ambiguus. A particularly powerful excitatory influence on unitary activity related to laryngeal adduction was produced by laryngeal stimuli; in many instances this influence could not be modified by other sensory inputs (e.g., from vagus or glossopharyngeal nerves). Laryngeal stimulation also produced a profound cessation of respiration and suppression of the inspiratory-related activity of laryngeal abductor units. Excitatory and inhibitory effects as a result of interacting various stimuli were also seen in recordings from motoneurons of the RLN and nucleus ambiguus. The effects described show characteristics similar to those noted in other oral-facial muscles and indicate common integrative and regulatory mechanisms. This study in the adult cat provides a basis of comparison for future studies in the kitten where the effects of laryngeal stimulation are augmented to such an extent that they have been implicated in disorders such as the sudden infant death syndrome (SIDS).

9: Cardiovascular changes associated with laryngeal stimulation and feeding in newborn lambs

9: Cardiovascular changes associated with laryngeal stimulation and feeding in newborn lambs

The effects of irritation at various levels of the airway upon tracheal mucus secretion in the cat.

1. Sulphated glycoprotein output from the trachea, isolated in situ, has been measured in anaesthetized cats by a radio-isotopic method. The effects of irritation of various parts of the airway on this mucus output were studied. 2. Mechanical stimulation of the nose and nasopharynx increased tracheal mucus output by reflexes which involved parasympathetic and probably also sympathetic motor pathways. 3. Laryngeal stimulation had a similar through the same motor pathways. 4. Inhalation of ammonia vapour into the lower airways reflexly increased mucus output from the isolated trachea. The efferent pathway for this reflex was mainly or entirely parasympathetic. It is argued that the afferent pathway involved cough receptors. 5. Lung inflation, inhalation of histamine aerosol and intravenous injection of phenyl diguanide (which excite mainly lung stretch receptors, lung 'irritant' receptors and alveolar 'J-receptors' respectively) had no consistent effect on tracheal mucus secretion. 6. The afferent and efferent pathways of these reflexes are discussed.

Reflex swallowing elicited by water and chemical substances applied in the oral cavity, pharynx, and larynx of the rabbit.

Water and various chemical solutions were applied to the oral cavity, pharynx, and larynx of anesthetized rabbits to study their effects on the swallowing reflex. Laryngeal stimulation: Water was an effective stimulus in eliciting reflex swallowing; NaCL depressed this reflex. The effect of salt solutions on swallowing was dependent on anion species. Weakly hydrated anions had a depressing effect while greatly hydrated anions had a facilitating effect. The order of the depressing effect of the anions was Br-greater than SCN- greater than CL- congruent to NO3 -, and the order of the facilitating effect of anions was citrate greater than SO42 - greater than HCO3-. Oral and pharyngeal stimulation: Water elicited swallowing; however, this effect was less marked than that in the larynx. NaCL in concentrations lower than 200 mM had a depressing effect while at higher concentration it had a facilitating effect. Sucrose, acetic acid, and alcohol evoked successive swallowing in the first two or three trials. It was found that water applied to the laryngeal region had the marked effect of eliciting reflex swallowing and that most gustatory substances infused into the oral and pharyngeal regions had a facilitating effect on the initation of swallowing.

Reflex of the Tracheobronchial Smooth Muscle to Nasal Mucosa Stimulation

In an attempt to reveal the reflex mechanism of the tracheobronchial smooth muscle to stimuli to the nasal and laryngeal mucosa, experiments were performed using dogs. The method employed consisted of mechanical plethysmography and measurement of total lower pulmonary resistance. The following results were obtained. 1. A clear reflex relationship exists between the nasal mucosa and the tracheobronchial muscle, and also between the laryngeal mucosa and the tracheobronchial muscle. 2. Stimulation of the nose, irrespective of its intensity, nature, or the site stimulated, always caused reflex dilatation of the tracheobronchial lumen, when the stimulus was above threshold level. Stimulation of the larynx caused reflex contraction of the tracheobronchial lumen, although on rare occasions it caused dilatation. 3. The degree of response to nasal and laryngeal stimulation depended greatly on the pre-stimulatory level of tonus of the tracheobronchial muscle. It was noted that the greater the response of the tracheobronchial muscle to laryngeal stimulation, the less is the response to nasal stimulation, and vice versa .

Effect of microaerosol inhalation on the pattern of breathing.

Microaerosol stimulation of the trachea and bronchi appears to have no effect on the pattern of breathing. However, laryngeal stimulation with microaerosol produces consistent changes characterized by slowing of the inspiratory effort. The reflex response can be abolished by either bilateral superior laryngeal nerve section or topical anesthesia of the laryngeal mucous membranes. Nasal stiumulation with saline microaerosol results in marked slowing of inspiration. This response can also be blocked by topical anesthesia of the nasal mucosa. The decreased breathing rate results from both increased t insp. and t exp. During inspiration the build-up phrenic discharge activity, the phrenic slope, decreases. The phrenic peak, however, remains unchanged. The nose and larynx, therefore, appear to play significant roles in the modification of the breathing pattern in response to a nonirritating solution delivered as a microaersol. Slower breathing, relexly produced in the human being by such a method, might benefit partial airway obstruction by reducing turbulence and therefore the work of breathing. It is speculated that in a marginally competent upper airway, this benefit might be a critical factor in survival.

Activity in single hypoglossal fibers during cortically induced swallowing and chewing in rabbits

In rabbits under light ether anesthesia, rhythmic movements of chewing and swallowing were produced by stimulation to the antero-lateral cortex. The activity of hypoglossal motor fibers during such stimulation was studied, together with changes evoked by stimulation of the superior laryngeal nerve. 1. Most hypoglossal motor fibers discharged bursts of impulses in phase with the cortically evoked rhythmic chewing, the majority being concurrent with jawclosing. Among these, some units fired with fairly constant latency after each stimulus, while others had no consistent relation to the stimuli in the train. A few units bore no relation to the rhythm of chewing in their discharge of impulses, either following regularly to each stimulus or occurring sporadically. 2. In the hypoglossal units discharging grouped impulses in phase with chewing, some displayed also a characteristic burst, whereas others ceased discharging momentarily when a swallow occurred during cortical stimulation. 3. The shortest time for cortico-hypoglossal conduction ranged from 5.8 to 12.0 msec, indicating polysynaptic linkage for the path. 4. Cortically evoked rhythmic chewing was arrested by stimulation of the superior laryngeal nerve. During this period, one group of hypoglossal units ceased discharging completely, while others discharged impulses regularly after each stimulus pulse. 5. Motoparalysis did not alter the pattern of discharge of the hypoglossal nerve fibers by cortical and/or superior laryngeal stimulation, though abolishing totally the movement of chewing and swallowing. 6. The relevance of these findings to the central neural arrangement for the control of rhythmic chewing and swallowing is discussed.