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J Appl Physiol 95: 1759-1760, 2003; doi:10.1152/japplphysiol.00747.2003
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INVITED EDITORIAL

Upper airway surface tension: is it a significant cause of airflow obstruction during sleep?

Alan R. Schwartz, Hartmut Schneider, and Philip L. Smith

Johns Hopkins Sleep Disorders Center Johns Hopkins School of Medicine Baltimore, Maryland 21224

OBSTRUCTIVE SLEEP APNEA IS characterized by repetitive episodes of upper airway obstruction during sleep, leading to oxyhemoglobin desaturation, recurrent arousals, and long-term neurocognitive, metabolic, and cardiovascular dysfunction. It is widely recognized that this disorder is due to alterations in the control of upper airway patency during sleep (16). Among the factors leading to upper airway collapse and airflow obstruction, alterations in airway structures and/or disturbances in neuromuscular control are thought to play major roles (6, 12). Recent work by Kirkness and others (8–11) suggests that surface tension plays a role in modulating upper airway patency and may also be a marker for disturbances in airway neuromuscular control.

A number of structural alterations are thought to compromise airway patency and predispose to increasing degrees of airflow obstruction during sleep. Bulk changes in soft tissue mass, anatomic narrowing by bony structures, and decreases in axial tension have all been associated with reductions in upper airway patency in animals and humans (17, 19). Each of these factors leads to a loss in forces that either tether upper airway structures open or stretch the luminal surface longitudinally, making it more resistant to collapse (17). Structural defects caused by microagnathia, fatty deposits, soft tissue infiltration, and the loss of caudal trachea traction have all been demonstrated to increase upper airway collapsibility, resistance, compliance, or luminal cross-sectional area (1).

Recent studies by Kirkness and coworkers (8–11) have now added surface tension in upper airway lining fluid to the list of structural factors that influence airway patency. In an extensive series of experiments, these investigators have systematically explored the effects of surface-acting forces on upper airway function in animals and humans. Their work was prompted by earlier observations that surfactant might help restore upper airway patency and reduce collapsibility in animals (13) and awake humans (18). Kirkness and coworkers (8) initially developed an elegant technique for measuring surface tension in scant amounts of upper airway lining fluid and demonstrated a strong correlation between changes in upper airway collapsibility and surface tension induced by surfactant and saline instillation. In studies in anesthetized rabbits and humans, they demonstrated that surfactant improved upper airway patency, as reflected by decreases in critical opening pressures and upstream resistance, and that it decreased the hysteresis between upper airway opening and closing pressures (9, 10).

The authors' most recent study, which appears in this issue of the Journal (see Ref. 11), extends their work in anesthetized rabbits and humans to the sleeping human with intact airway neuromuscular control mechanisms. Examining the effect of surfactant instillation, they demonstrated significant decreases in the surface tension of pharyngeal lining fluid, upper airway collapsibility, and sleep apnea severity (respiratory disturbance index). Observed improvements in sleep apnea severity were primarily related to decreases in hypopneas in their patient group, which correlated with reductions in surface tension. This study provides firm evidence that surface tension plays a role in the regulation of airway patency and may influence sleep apnea severity.

An intriguing finding was that improvements in the sleep apnea severity correlated with the decrease in surface tension after surfactant instillation. This relationship is consistent with the notion that surface tension may vary substantially between individuals and may either predispose to or protect against sleep apnea. In fact, surface tension can vary over a relatively wide range, from 50 to 90 mN/m among study subjects (10). Although the mechanism for variability in surface tension is unclear, differences in salivary flow, route of breathing, and/or pharyngeal mucosal properties may play a role. Recurrent mucosal trauma from continuous snoring and inspiratory flow limitation during sleep may dry the mucosa excessively and adversely elevate surface tension. Thus a vicious circle of decreasing surface tension leading to worsening airflow obstruction, mucosal trauma, and further increases in sleep apnea severity may result. Moreover, dessication of the pharyngeal lining may account for alterations in local sensory receptors, which have recently been demonstrated to play a role in maintaining airway patency (7).

Is there a role for measurements of surface tension and surfactant instillation in the management of sleep apnea? The effects of surfactant can be gauged from critical pressure measurements pre- and postinstillation. The findings of Kirkness et al. (11) demonstrate that critical pressures can decrease by 2–3 cmH2O after surfactant administration. Relatively modest reductions in critical pressure of this magnitude would be expected to decrease hypopnea frequencies but have little effect on apnea frequencies (5), as confirmed by these authors. Decreases in critical pressure up to 3 cmH2O are comparable to those previously observed with changes in body position (2, 14) and might represent an adjunct to therapy for sleep apnea patients. Moreover, decreases in critical pressure of this magnitude should be effective in relieving upper airway resistance syndrome and/or diminishing snoring intensity in those without sleep-disordered breathing (3, 4). Finally, measurements of upper airway surface tension might guide clinicians in deploying surfactant therapy and might be used as a marker for mucosal injury and sensory receptor dysfunction in this disorder (15). Further work is required to correlate surface tension in upper airway lining fluid with altered structural changes and sensorineural defects in upper airway control.


   FOOTNOTES
 

E-mail: aschwarz{at}jhmi.edu

REFERENCES

  1. Ayappa I and Rapoport DM. The upper airway in sleep: physiology of the pharynx. Sleep Med Rev 7: 9-33, 2003.
  2. Boudewyns A, Punjabi N, Van de Heyning PH, De Backer WA, O'Donnell CP, Schneider H, Smith PL, and Schwartz AR. Abbreviated method for assessing upper airway function in obstructive sleep apnea. Chest 118: 1031-1041, 2000.
  3. Gleadhill IC, Schwartz AR, Schubert N, Wise RA, Permutt S, and Smith PL. Upper airway collapsibility in snorers and in patients with obstructive hypopnea and apnea. Am Rev Respir Dis 143: 1300-1303, 1991.
  4. Gold AR, Marcus CL, Dipalo F, and Gold MS. Upper airway collapsibility during sleep in upper airway resistance syndrome. Chest 121: 1531-1540, 2002.
  5. Gold AR and Schwartz AR. The pharyngeal critical pressure. The whys and hows of using nasal continuous positive airway pressure diagnostically. Chest 110: 1077-1088, 1996.
  6. Isono S, Remmers JE, Tanaka A, Sho Y, Sato J, and Nishino T. Anatomy of pharynx in patients with obstructive sleep apnea and normal subjects. J Appl Physiol 82: 1319-1326, 1997.
  7. Kimoff RJ, Sforza E, Champagne V, Ofiara L, and Gendron D. Upper airway sensation in snoring and obstructive sleep apnea. Am J Respir Crit Care Med 164: 250-255, 2001.
  8. Kirkness JP, Amis TC, Wheatley JR, and Christenson HK. Determining the surface tension of microliter amounts of liquid. J Colloid Interface Sci 232: 408-409, 2000.
  9. Kirkness JP, Christenson HK, Garlick SR, Parikh R, Kairaitis K, Wheatley JR, and Amis TC. Decreased surface tension of upper airway mucosal lining liquid increases upper airway patency in anaesthetised rabbits. J Physiol 547: 603-611, 2003.
  10. Kirkness JP, Eastwood PR, Szollosi I, Platt PR, Wheatley JR, Amis TC, and Hillman DR. Effect of surface tension of mucosal lining liquid on upper airway mechanics in anesthetized humans. J Appl Physiol 95: 357-363, 2003.
  11. Kirkness JP, Madronio M, Stavrinou R, Wheatley JR, and Amis TC. Relationship between surface tension of upper airway lining liquid and upper airway collapsibility during sleep in obstructive sleep apnea hypopnea syndrome. J Appl Physiol 95: 1761-1766, 2003.
  12. Mezzanotte WS, Tangel DJ, and White DP. Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism). J Clin Invest 89: 1571-1579, 1992.
  13. Miki H, Hida W, Kikuchi Y, Chonan T, Satoh M, Iwase N, and Takishima T. Effects of pharyngeal lubrication on the opening of obstructed upper airway. J Appl Physiol 72: 2311-2316, 1992.
  14. Neill AM, Angus SM, Sajkov D, and McEvoy RD. Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea. Am J Respir Crit Care Med 155: 199-204, 1997.
  15. Paulsen FP, Steven P, Tsokos M, Jungmann K, Muller A, Verse T, and Pirsig W. Upper airway epithelial structural changes in obstructive sleep-disordered breathing. Am J Respir Crit Care Med 166: 501-509, 2002.
  16. Remmers JE, deGroot WJ, Sauerland EK, and Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 44: 931-938, 1978.
  17. Rowley JA, Permutt S, Willey S, Smith PL, and Schwartz AR. Effect of tracheal and tongue displacement on upper airway airflow dynamics. J Appl Physiol 80: 2171-2178, 1996.
  18. Van der Touw T, Crawford AB, and Wheatley JR. Effects of a synthetic lung surfactant on pharyngeal patency in awake human subjects. J Appl Physiol 82: 78-85, 1997.
  19. Watanabe T, Isono S, Tanaka A, Tanzawa H, and Nishino T. Contribution of body habitus and craniofacial characteristics to segmental closing pressures of the passive pharynx in patients with sleep-disordered breathing. Am J Respir Crit Care Med 165: 260-265, 2002.




This Article
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Right arrow Articles by Schwartz, A. R.
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