The effects of lung reflexes on laryngeal resistance and motoneurone discharge

Stránský, A; Szereda-Przestaszewska, Małgorzata; Widdicombe, J. G.

doi:10.1113/jphysiol.1973.sp010241

Cited by 77 publications

(31 citation statements)

References 15 publications

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“…1 and 3) may be related to the fact that airway pressure peaks earlier in the PS mode. As recently reviewed (2), available but scarce data suggest that, while stimulation of slow adapting receptors inhibits TA EMG (5, 13), stimulation of rapidly adapting receptors or C fibers could enhance phasic TA EMG, although in the expiration phase (14,45). Alternatively, increased afferent activity from positive pressure receptors in the upper airways (pharynx and/or larynx) (33,43) could be involved in the activation of inspiratory TA EMG, as suggested by recent results from experiments on isolated larynx in piglets (44).…”

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confidence: 99%

Laryngeal response to nasal ventilation in nonsedated newborn lambs

Moreau-Bussière¹,

Samson²,

St-Hilaire³

et al. 2007

Journal of Applied Physiology

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Although endoscopic studies in adult humans have suggested that laryngeal closure can limit alveolar ventilation during nasal intermittent positive pressure ventilation (nIPPV), there are no available data regarding glottal muscle activity during nIPPV. In addition, laryngeal behavior during nIPPV has not been investigated in neonates. The aim of the present study was to assess laryngeal muscle response to nIPPV in nonsedated newborn lambs. Nine newborn lambs were instrumented for recording states of alertness, electrical activity [electromyograph (EMG)] of glottal constrictor (thyroarytenoid, TA) and dilator (cricothyroid, CT) muscles, EMG of the diaphragm (Dia), and mask and tracheal pressures. nIPPV in pressure support (PS) and volume control (VC) modes was delivered to the lambs via a nasal mask. Results show that increasing nIPPV during wakefulness and quiet sleep led to a progressive disappearance of Dia and CT EMG and to the appearance and subsequent increase in TA EMG during inspiration, together with an increase in trans-upper airway pressure (TUAP). On rare occasions, transmission of nIPPV through the glottis was prevented by complete, active glottal closure, a phenomenon more frequent during active sleep epochs, when irregular bursts of TA EMG were observed. In conclusion, results of the present study suggest that active glottal closure develops with nIPPV in nonsedated lambs, especially in the VC mode. Our observations further suggest that such closure can limit lung ventilation when raising nIPPV in neonates. thyroarytenoid muscle; cricothyroid muscle; diaphragm; states of alertness; intermittent positive-pressure ventilation NASAL INTERMITTENT positive-pressure ventilation (nIPPV) is increasingly used in the neonatal period (12) as treatment for respiratory distress syndrome (22) and apneas of prematurity (3,27) and as a bridge between endotracheal tube ventilation and spontaneous ventilation (6,19). Previous studies using endoscopic observations in adult humans have shown that laryngeal closure can occur during nIPPV, especially in the volume control (VC) mode (17, 18, 34 -36). In addition, laryngeal closure appears to increase with increasing ventilatory support, together with decreasing subglottal (alveolar) ventilation (40). Such laryngeal behavior is of high clinical importance since it has been linked to falls in oxygen saturation when increasing nIPPV during sleep in adult humans (7) and could divert positive pressure from the airways, leading to increased gastric distension (11). However, although the glottal closure observed endoscopically during nIPPV suggests an active contraction of glottal constrictor muscles, there are, to our knowledge, no data on glottal muscle electromyograms (EMG) during nIPPV. Moreover, there are no currently available studies on laryngeal dynamics during nIPPV in the neonatal period. Thus the aim of the present study was to test the hypotheses that 1) glottal narrowing during nIPPV is also present in the neonatal period, especially in the VC mode; and 2) glottal...

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confidence: 99%

Laryngeal response to nasal ventilation in nonsedated newborn lambs

Moreau-Bussière¹,

Samson²,

St-Hilaire³

et al. 2007

Journal of Applied Physiology

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“…In this respect it is known that both 'lung irritant receptors' [Mills, Sellick and Widdicombe, 1969] and alveolar nociceptive (type J) [Paintal, 1969] endings can cause a reflex laryngeal constriction [Stransky et al, 1973]. Stimulation of either or both of these groups of endings by veratrine might therefore account for our results.…”

Section: Discussionmentioning

confidence: 38%

“…In a previous paper we have described the pressure/flow relationship of the cat larynx, and have shown that laryngeal constriction is produced by chemical stimulation of lung irritant receptors in the airway epithelium and alveolar nociceptive (type J) receptors [Stransky et al, 1973]. The method of assessing laryngeal resistance with the larynx 'out of circuit' gives a direct indication of resistance changes; with the larynx 'in circuit' the measured resistances will depend on the rate of airflow, which may tend to keep the larynx open passively.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Intravascular Injections of Veratrine on Laryngeal Resistance to Airflow in Cats

Szereda‐Przestaszewska¹,

Widdicombe²

1973

Exp Physiol

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Changes in laryngeal resistance to airflow have been measured in cats during spontaneous breathing through the larynx, and while the larynx was isolated in 8itU 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.Many papers deal with the veratrum alkaloids and their influence on the cardiovascular and respiratory systems [Dawes and Comroe, 1954] and the hypotension, bradycardia and arrest of breathing induced by intravenous injections of veratrum alkaloids, classically described by Bezold and Hirt [1867], are known to depend on vagal reflexes. The inhibition of respiration caused by veratrine -a mixture of veratrum alkaloids -was studied by Dawes, Mott and Widdicombe [1951] who showed that the apnoea observed in cats with small doses of veratridine (a pure alkaloid) is blocked by cooling the vagi to 10TC, and that the lung receptors responsible for this response are the pulmonary stretch endings. These investigations were complemented by recordings of the activity of single fibres from pulmonary stretch receptors, which showed after veratridine injection an increased frequency in the inspiratory volleys, and tonic, frequency modulated activity, coupled with slowing of breathing. This has been confirmed for rabbits [Meier, Bein and Helmich, 1949], cats [Paintal, 1953] and guinea pigs [Zipf and Marquardt, 1966]. Thus the vagal pathway for the inhibitory effects of veratrum alkaloids on breathing is well established [see also Herzog, 1958; Hapke, 1963a and b].The reflex cardiovascular actions of injections of veratrine are mediated mainly by stimulation of receptors in the muscle of the ventricles of the heart, probably with nonmyelinated vagal fibres [Sleight and Widdicombe, 1965].In previous experiments we have found increases in laryngeal resistance in expiration with induction of respiratory reflexes from the lungs and the upper airways [Stransky, Widdicombe, 1972, 1973] and have here tried to relate the respiratory changes induced by veratrine to quantitative measurements of laryngeal resistance to airflow.

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“…Laryngeal muscle contraction as a result of vagal stimulation is the expected result (Stransky et al 1973). Most previous studies suggested that stimulation of vagus nerves or electrical field stimulation of airway tissue results in contraction of lower airways muscles which are blocked by atropine (Widdicombe 1986a, b).…”

Section: Discussionmentioning

confidence: 98%

“…As is well known, the recurrent laryngeal nerve, which is responsible for the motor innervation of the larynx, leaves vagus at the upper thoracic region and goes to the larynx (Stransky et al 1973;Widdicombe 1986a, b). The decrease in BP depends on the general cardiovascular response.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Vagal Stimulation on Laryngeal Vascular Resistance and Intraluminal Pressure in the Dog

Yelmen

Şahin

Oruc

2004

Tohoku J. Exp. Med.

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In anaesthetized dogs (sodium pentobarbitone 30 mg/kg, i.v.) laryngeal vascular resistance was measured by unilateral perfusion at constant flow of the branch of the cranial superior thyroid artery that supplies the larynx. Arterial perfusion was at constant flow and inflow pressure was divided by flow to give laryngeal vascular resistance (R LV ). Intraluminal laryngeal pressure (P L ) and systemic arterial blood pressure (BP) were also measured. Stimulation (20 V, 20 Hz, 0.2 milliseconds) of the central end of cervical vagus caused an increase in R LV (+22.9±6.1%) and a decrease in P L (−12.1±4.4%). Stimulation (10 V, 10 Hz, 0.2 milliseconds) of the central end of the recurrent laryngeal nerve (RLN) reduced R LV (−3.4±0.8%) and P L (−7.5±4.1%). Stimulation of the peripheral end of the RLN decreased R LV (−7.1±1.9%) and increased P L (+21.6±7.7%). Stimulation of the central end of the superior laryngeal nerve (SLN) increased R LV (+17.9±3.2%) and P L (+59.8±2.7%), whereas stimulation of the peripheral end of the SLN decreased R LV (-4.8±1.6%) and P L (−4.1±2.4%). After treatment with α -adrenoreceptor antagonist phentolamine (0.5 mg/kg, i.v.), stimulation of the central end of cervical vagus nerve reduced R LV by 25% and decreased BP. Phentolamine caused a decrease in BP and reduced the magnitude of increase in R LV in response to stimulation of central end of SLN. After atropine sulphate (0.5-2.0 mg/kg, i.v.), the stimulation of both central and peripheral ends of RLN reduced R LV . The decrease in R LV during stimulation of peripheral end of SLN was reduced by atropine. Thereafter, pancuronium bromide (0.06-0.1 mg/kg, i.v.) was given and dogs were artifically ventilated. After paralyzed, stimulation of the central end of the SLN decreased R LV (+26.0±4.5%) but produced no change in P L . It is concluded that parasympathetic motor fibers in the RLN and SLN are effective for the laryngeal vascularity and non-adrenergic system may be responsible for laryngeal vasoconstriction. laryngeal vasculature; vagal stimulation; phentolamine; atropine

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The effects of lung reflexes on laryngeal resistance and motoneurone discharge

Cited by 77 publications

References 15 publications

Laryngeal response to nasal ventilation in nonsedated newborn lambs

Laryngeal response to nasal ventilation in nonsedated newborn lambs

The Effect of Intravascular Injections of Veratrine on Laryngeal Resistance to Airflow in Cats

The Effects of Vagal Stimulation on Laryngeal Vascular Resistance and Intraluminal Pressure in the Dog

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