Increase In Laryngeal Resistance Research Articles

Effects of Bilateral Arytenoid Cartilage Stenting on Canine Laryngeal ResistanceEx Vivo

To evaluate the effect of Nitinol stents for bilateral arytenoid lateralization on canine laryngeal resistance. Ex vivo experimental study. Canine cadaver larynges (n=7). Laryngeal resistance was calculated in all specimens with the epiglottis in open and closed positions. Bilateral arytenoid stenting was performed, rima glottidis width measured, and laryngeal resistance calculated. The effects of stenting on laryngeal resistance were evaluated by repeated measures ANOVA. Calculated laryngeal resistance in the 3 stented groups, 2 cm (0.034±0.059 cmH(2) O/L/s), 3 cm (0.034±0.059 cmH(2) O/L/s), and 4 cm (0.034±0.059 cm H(2) O/L/s), was significantly decreased versus the control (unstented) group (0.947±0.624 cmH(2) O/L/s; P=.0098) with an epiglottis in the normal position. Calculated laryngeal resistance in the 3 stented groups, 2 cm (43.407±17.348 cm H(2) O/L/s), 3 cm (70.659±34.705 cmH(2) O/L/s), and 4 cm (92.637±44.509 cm H(2) O/L/s), was significantly increased versus the control (unstented) group (29.561±14.499 cm H(2) O/L/s) (P=.0185) with an epiglottis in the closed position. The width of the rima glottidis correlated with the size of the stent (r=0.95, P<.001). Bilateral arytenoid stenting significantly reduced calculated laryngeal resistance with an open epiglottis. Stenting resulted in a significant increase in laryngeal resistance versus the control with a closed epiglottis. Use of bilateral arytenoid stenting in clinical cases of laryngeal paralysis may provide an adequate decrease in open-epiglottis airway resistance to alleviate clinical signs, while increasing closed-epiglottis airway resistance. This could potentially lead to a decrease in the risk of postoperative aspiration pneumonia.

Pathogenesis of laryngeal narrowing in patients with multiple system atrophy

1. We do not fully understand the pathogenesis of nocturnal laryngeal stridor in patients with multiple system atrophy (MSA). Recent studies suggest that inspiratory thyroarytenoid (TA) muscle activation has a role in the development of the stridor. 2. The breathing pattern and firing timing of TA muscle activation were determined in ten MSA patients, anaesthetized with propofol and breathing through the laryngeal mask airway, while the behaviour of the laryngeal aperture was being observed endoscopically. 3. Two distinct breathing patterns, i.e. no inspiratory flow limitation (no-IFL) and IFL, were identified during the measurements. During IFL, significant laryngeal narrowing was observed leading to an increase in laryngeal resistance and end-tidal carbon dioxide concentration. Development of IFL was significantly associated with the presence of phasic inspiratory activation of TA muscle. Application of continuous positive airway pressure suppressed the TA muscle activation. 4. The results indicate that contraction of laryngeal adductors during inspiration narrows the larynx leading to development of inspiratory flow limitation accompanied by stridor in patients with MSA under general anaesthesia.

Differential effects of hypercapnia on expiratory phases of respiration in the piglet

Hypercapnia induces prolongation of expiratory time (T e) during early development. In the present study, we determined the response to steady state hypercapnia of three neural phases of the total respiratory cycle, inspiration (T i), stage 1 or passive expiration, T e-1 and stage 2 or active expiration, T e-2. Experiments were performed in decerebrate, vagotomized, spontaneously breathing piglets aged 5–10 days. Neural phases of the respiratory cycle were based on electrical activities of the thyroarytenoid (TA, laryngeal adductor) and triangularis sternii (TS, chest wall expiratory muscle) in relation to diaphragm (D) activity. We observed that hypercapnia induced prolongation of both expiratory phases. The greater prolongation of T e-1 was associated with an increase in TA activity and an increase in laryngeal resistance, which peaked early in T e-1, and then progressively decreased. These findings demonstrate that, in early postnatal life, a hypercapnia induced increase in respiratory drive is associated with centrally mediated prolongation of both phases of expiration, a greater prolongation of T e-1, and an increase in laryngeal resistance during post-inspiration. We speculate that the latter serves to optimize gas exchange by reducing large fluctuations in functional residual capacity.

Similarities in reflex control of laryngeal and cardiac vagal motor neurones

We sought to test the hypothesis that laryngeal adductor and cardiac vagal motor neurones respond similarly to the activation of certain afferent inputs. Experiments were performed on a working heart–brainstem preparation of rat devoid of pulmonary stretch receptor feedback. Upper airway negative pressure receptors (UANPR), peripheral arterial chemoreceptors and receptors at the junction of the pharynx and oesophagus were stimulated selectively while recording heart rate, recurrent laryngeal, phrenic and hypoglossal motor outflows, subglottic pressure during constant translaryngeal airflow (as an index of laryngeal resistance), and single unit respiratory neurone activity. Stimulation of all three receptor types produced bradycardia, evoked discharges in the recurrent laryngeal and hypoglossal motor outflows during the post-inspiratory period and caused swallowing. Stimulation of pharyngoesophageal receptors and peripheral chemoreceptors evoked an increase in laryngeal resistance during the post-inspiratory phase indicative of laryngeal adductor motoneurone activation. Although this reflex response cannot be evaluated during UANPR stimulation, some post-inspiratory neurones were powerfully activated suggesting that UANPR probably drive laryngeal adductor muscles. Our data show that motor outflows controlling cardiac rate and laryngeal patency are concurrently activated by these sensory inputs. This may constitute the basis for a stereotyped defensive reflex response which maintains end expiratory lung volume, thus conserving oxygen in conditions of upper airway obstruction. Our observations lend further support to models of cardiorespiratory control which propose close coupling and shared central mechanisms for the regulation of the cardiovascular and respiratory systems.

Ventilatory and upper-airway resistance responses to upper-airway cooling and CO2 in anaesthetised rats.

The effects of upper airway (UA) cool air and CO2 on breathing and on laryngeal and supraglottic resistances were studied in anaesthetised rats breathing spontaneously through a tracheostomy. Warm, humidified air containing 0, 5 and 9-10% CO2 and cool, room-humidity air were delivered at constant flow to either the isolated larynx to exit through a pharyngotomy or to the supraglottic UA to exit through the mouth and/or nose (nose open or sealed). Spontaneous tracheal airflow and UA airflows, temperatures and pressures were recorded. CO2 had no effect on breathing but caused a slight increase in laryngeal resistance which was abolished by cutting the superior laryngeal nerves (SLN). Cool air caused a decrease in respiratory frequency and/or peak inspiratory flow when applied to the isolated larynx or to the supraglottic airway with the nose closed. These effects were abolished by SLN section. With the nose open, the ventilatory inhibition was not abolished by SLN section. Cool air also caused substantial decreases in laryngeal and supraglottic resistances which were attenuated by SLN section and which persisted following recurrent laryngeal nerve section. In conclusion, whilst UA cooling inhibits breathing and decreases UA resistances, UA CO2 has minimal effects.

Laryngeal resistance immediately after panting in asthmatic subjects.

The panting manoeuvre may be used during the assessment of airway resistance and in asthmatic patients during bronchial provocation testing or spontaneous asthma. To study whether panting opens the larynx in patients with asthma, laryngeal resistance was examined in six patients with stable asthma before and after methacholine induced bronchoconstriction and in another six patients with spontaneous asthma. Subjects were asked to pant and then to hold their breath immediately afterwards. Laryngeal resistance after panting was compared to that during quiet tidal breathing. Change in laryngeal resistance was estimated by a method using low frequency sound and respiratory resistance by forced oscillation at 10 Hz. Mean baseline respiratory resistance during inspiration was 0.245 and 0.470 kPa/l.s before and after methacholine in the patients with stable asthma and 0.480 kPa/l.s in the patients with spontaneous asthma. In the patients with stable asthma mean laryngeal resistance was lower after panting than during the preceding quiet tidal breathing, both before and after methacholine induced bronchoconstriction (by 0.08 before and by 0.065 kPa/l.s after). In contrast, the patients with spontaneous asthma showed an increase in laryngeal resistance after panting of 0.089 kPa/l.s. The magnitude of change in laryngeal resistance after panting was similar to the change in respiratory resistance in the patients with spontaneous asthma and in the patients with stable asthma after methacholine, but was greater than the change in respiratory resistance in the patients with stable asthma before methacholine. These results suggest that panting may cause different effects on the laryngeal aperture in patients with stable and spontaneous asthma.

Upper airway resistances in fetal sheep: the influence of breathing activity.

Fetal breathing movements (FBM) and lung liquid volume are known to affect lung development, but little is known about mechanisms controlling movement of liquid through the upper respiratory tract (URT). Therefore we measured resistances of the URT in 8 unanesthetized fetal sheep during late gestation while FBM were monitored from pressures in the lower trachea or from electromyogram of respiratory muscles. URT resistance to liquid flow toward the amniotic sac increased from 3.5 +/- 1.9 Torr X ml-1 X min during episodes of FBM to 21.1 +/- 5.7 Torr X ml-1 X min during apnea. Laryngeal resistance during apnea was greater (P less than 0.001) than supralaryngeal resistance in each of six fetuses in which URT resistance was partitioned. Fetal paralysis abolished the increase in laryngeal resistance to efflux that was previously related to the high-voltage electrocortical state and apnea. We were unable to quantify URT resistance to fluid movement toward the lungs because the larynx acted as a valve, permitting flow toward the lungs only in the presence of FBM. The supralaryngeal portion of the URT also apparently acts as a valve, normally preventing the entry of amniotic fluid into the pharynx. These findings help to explain our earlier observations that efflux of liquid from the fetal lungs is greater during episodes of FBM than during apnea.

Opioids increase laryngeal resistance and motoneuron activity in the recurrent laryngeal nerve

[D-Ala 2, Met 5]enkephalinamide (DAME), [D-Ala 2, Leu 5]enkephalinamide (DALE) and morphine sulfate (MS) increase activity in the recurrent laryngeal nerve (RLN) within 1 s subsequent to right atrial administration. The activation of the RLN was correlated with a large increase in the resistance to airflow in the in situ isolated larynx. Single unit recurrent laryngeal motoneuron recordings showed that the increase in laryngeal resistance was caused by the continuous activation and recruitment of expiratory motoneurons. Results obtained with opioids mimicked those of phenydiguanide (20–40 μg/kg RA), an agent known to stimulate pulmonary J-receptors. Opioid-induced increases in laryngeal resistance were blocked by bilateral section of the RLN and pretreatment with naloxone (100 μg/kg RA). Naloxone had no effect on PDG responses. During the initial period of laryngeal motoneuron activation, the phrenic nerve (PN) was inhibited, however, the activation of the RLN was not dependent upon PN inhibition. It was concluded that stimulation of pulmonary opiate receptors, which may be associated with vagal afferents, elicit a reflex activation of expiratory recurrent laryngeal motoneurons resulting in an increase in laryngeal resistance.

Laryngeal Regulation of Airway Resistance

The response of laryngeal airway resistance to pulmonary receptor stimulation was studied in 20 mongrel dogs anesthetized with alpha-chloralose (80 mg/kg). Stimulation of pulmonary stretch receptors by lung inflation inhibited the phasic variation of laryngeal resistance during respiration and produced a sustained reduction of laryngeal resistance, which was related to lung inflation pressure. Stimulation of pulmonary J-receptors with capsaicin produced apnea and a large increase in laryngea resistance. Capsaicin produced this reflex when injected into the pulmonary circulation but not when injected into the systemic circulation. Irritant receptor stimulation with histamine hydrochloride produced tachypnea and a reduction in inspiratory laryngeal resistance. Pulmonary receptor reflexes were abolished by dividing the vagus nerves distal to the origin of the recurrent laryngeal nerves. Laryngeal reflexes may be important in the regulation of respiration and the production of physiologic and pathologic alterations in pumonary function.

The effect of intravascular injections of veratrine on laryngeal resistance to airflow in cats.

Changes in laryngeal resistance to airflow have been measured in cats during spontaneous breathing through the larynx, and while the larynx was isolated in situ with constant airflow. Intravenous injections of veratrine resulted in apnoea with a large increase in laryngeal resistance, followed by expiratory increases in laryngeal resistance. These responses were abolished by cutting the vagi in the chest and were absent on injection of veratrine into the left atrium, which established the pulmonary nerves as the main afferent pathway for the reflex. It is concluded that stimulation of pulmonary receptors constricts the larynx.

Reflex effects of chemical irritation of the upper airways on the laryngeal lumen in cats

Changes in airflow resistance of the larynx isolated in situ have been measured in spontaneously breathing cats, vagotomised in the chest, during chemical stimulation of the nose and larynx. Insufflation of ammonia vapour into the larynx inhibited breathing with a large increase in expiratory laryngeal resistance. These responses were abolished by cutting the superior laryngeal nerves, which established the afferent path for the reflex. Insufflation of ammonia into the nose caused sneezing or inhibition of breathing with expiratory increases in laryngeal resistance, which were smaller after sensory denervation of the larynx. The main afferent pathway for this reflex is probably in the trigeminal nerves. The laryngeal reflexes were generally more sensitive than those with the same stimuli affecting breathing.

Effect of acute exposure to CO 2 on lung mechanics in normal man

The effect of CO 2 on lung mechanics was examined in 10 healthy men at rest. Measurements were begun after each breathed an inspired concentration of 6 % CO 2 in air for 5 min. Lung volumes, expiratory flow-volume curves, static pressure-volume curves of the lung, and pulmonary conductance were measured. CO 2 breathing produced a small but statistically significant increase in total lung capacity. Pulmonary conductance measured by a flow-interruption technique increased markedly in one subject but decreased in all others. The decrease in conductance was not prevented by treatment with a bronchodilator and was considered the result of an increase in laryngeal resistance. There was no consistent effect of CO 2 breathing on any other parameter.