Effect of surfactant on pharyngeal mechanics in sleeping humans: implications for sleep apnoea

Morrell, Mary J.; Arabi, Yaseen M.; Zahn, Brian R.; Meyer, Keith C.; Skatrud, James B.; Badr, M. Safwan

doi:10.1183/09031936.02.00273702

Cited by 47 publications

(30 citation statements)

References 17 publications

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“…Surface adhesive forces tend to cause the soft palate to remain in opposition to the back of the tongue during mouth closure and may delay separation of these structures following mouth opening [72,158]. Manipulation of surface adhesive forces through instillation of exogenous surfactant and saline has been found to improve upper airway patency [84,122]. Neck extension facilitates airway opening, whereas neck flexion promotes airway closure [121,164].…”

Section: Static and Dynamic Properties Of The Upper Airwaymentioning

confidence: 98%

Mechanisms of sleep-disordered breathing: causes and consequences

Leung

Comondore

Ryan

et al. 2011

Pflugers Arch - Eur J Physiol

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Obstructive sleep apnea (OSA) is very common in the general population and is characterized by ineffective inspiratory efforts against a collapsed upper airway during sleep. Collapse occurs mainly at the level of the velopharynx and oropharynx due to a combination of predisposing anatomy and the withdrawal of pharyngeal dilator activity during sleep. Central sleep apnea (CSA) is a manifestation of chemoreflex control instability, leading to periods of inadequate respiratory drive sufficient to trigger breathing, usually alternating with periods of hyperventilation. While both forms of apnea are the result of differing pathophysiology, it has become increasingly clear that OSA and CSA often coexist in the same patient, the existence of one can predispose to the other, and that the two are not as distinct as previously thought. Both OSA and CSA exert a number of acute deleterious effects including intermittent hypoxia, arousals from sleep, and swings in negative intrathoracic pressure, which in turn lead to chronic physiologic consequences such as autonomic dysregulation, endothelial dysfunction, and cardiac remodeling. These underlying pathophysiological mechanisms provide a framework for understanding why OSA and CSA may predispose to cardiovascular diseases like ischemic heart disease and stroke.

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Section: Static and Dynamic Properties Of The Upper Airwaymentioning

confidence: 98%

Mechanisms of sleep-disordered breathing: causes and consequences

Leung

Comondore

Ryan

et al. 2011

Pflugers Arch - Eur J Physiol

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“…Previously we reported a relationship between the surface tension (γ) of the liquid lining the upper airway (UAL) and patency of the pharyngeal airway, especially under conditions of reduced or absent upper airway dilator muscle activity (Kirkness et al 2003 a , b , 2005 b ). Moreover, in patients with obstructive sleep apnoea hypopnoea syndrome (OSAHS), topical application of exogenous surfactant to the pharyngeal mucosa lowers surface tension, reduces the collapsibility of the upper airway during sleep, and results in a reduction in the severity of sleep disordered breathing (Jokic et al 1998; Morrell et al 2002; Kirkness et al 2003 c ). In anaesthetized rabbits, lowering the γ of UAL with exogenous surfactant reduces the intraluminal pressures at which the passive upper airway closes (Kirkness et al 2003 a ).…”

mentioning

confidence: 99%

Saliva production and surface tension: influences on patency of the passive upper airway

Lam

Kairaitis

Verma

et al. 2008

The Journal of Physiology

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Pharyngeal patency is influenced by the surface tension (γ) of the upper airway lining liquid (UAL), of which saliva is a major component. We investigated the influences of saliva production on γ of the UAL, and upper airway re-opening and closing pressures. In 10 supine, male, anaesthetized, tracheostomised, mechanically ventilated New Zealand White rabbits, we measured re-opening and closing of the passive isolated upper airway at baseline and following graded (cumulative) doses of methacholine or atropine. Upper airway liquid volume index (UALVI) was assessed using a standardized suction procedure (secretion weight obtained per second) expressed as the natural logarithm (LnUALVI). The γ of UAL samples were measured using the 'pull-off' force technique. Across all animals, baseline values were: LnUALVI −6.2 (−8.6 to −5.4) median (interquartile range), γ of UAL 58.9 (56.6-59.9) mN m −1 , re-opening 8.6 (6.9-11.1) cmH 2 O, and closing pressures 3.2 (1.8-5.7) cmH 2 O. LnUALVI increased by ∼0.17 per μg kg −1 methacholine and decreased by ∼0.14 per 100 μg kg −1 atropine (both P < 0.03, linear mixed effects modelling). Surface tension was unchanged by methacholine but increased by ∼0.6 mN m −1 per 100 μg kg −1 atropine (P < 0.004). When data were analysed across all animals, both re-opening and closing pressures increased as surface tension increased (by ∼0.4 cmH 2 O mN −1 and by ∼0.7 cmH 2 O mN −1 , respectively; both P < 0.05). We conclude that saliva production influences upper airway mechanical properties partly via alterations in γ of UAL. We speculate that in obstructive sleep apnoea, altered autonomic activity may reduce saliva production and increase surface tension of the upper airway lining liquid, thus increasing the likelihood of upper airway obstruction.

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“…In a randomised, placebo-controlled study including seven males with OSA, surfactant (1 ml) or saline was instilled via a pharyngeal catheter over 1 min for a single night [65]. RDI decreased significantly with surfactant treatment (from 79.7 to 59.6), but not with placebo.…”

Section: Surfactantmentioning

confidence: 99%

“…Fluticasone [60], xylometazoline [61], phosphocholinamin [62], and surfactant [65] all showed only very minor effects on OSA severity indices. Daytime sleepiness was only assessed in the study using xylometazoline, and did not improve after active treatment.…”

Section: Choosementioning

confidence: 99%

Pharmacological approaches to the treatment of obstructive sleep apnoea

Kohler

Bloch

Stradling

2009

Expert Opinion on Investigational Drugs

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ChooseBackground: Currently the treatment of choice for symptomatic obstructive sleep apnoea (OSA) is continuous positive airway pressure (CPAP). Some patients with OSA do not tolerate CPAP or have insufficiently severe symptoms to justify its use; for these patients, drug therapy would be a desirable potential therapeutic alternative. Objective: To summarize the current evidence on the effectiveness of drug therapy in patients with OSA. Methods: A systematic review of randomized controlled trials was performed to investigate the effects of drug therapy on OSA. Results/conclusions: Searches of bibliographical databases revealed 33 trials investigating the effects of 27 different drugs on OSA severity and/or symptoms. The mechanisms by which these drugs are supposed to improve OSA include, amongst others, an increase in tone of the upper airways, an increase in ventilatory drive, a reduction in airway resistance, and alterations in surface tension forces in the upper airway. In most of these studies there was no significant effect on OSA observed. However, there is evidence from a few small trials that some drugs, especially those thought to increase upper airway muscle tone, have the potential to reduce OSA severity; but further data from larger studies of adequate duration are needed.

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Effect of surfactant on pharyngeal mechanics in sleeping humans: implications for sleep apnoea

Cited by 47 publications

References 17 publications

Mechanisms of sleep-disordered breathing: causes and consequences

Mechanisms of sleep-disordered breathing: causes and consequences

Saliva production and surface tension: influences on patency of the passive upper airway

Pharmacological approaches to the treatment of obstructive sleep apnoea

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