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Decreased surface tension of upper airway mucosal lining liquid increases upper airway patency in anaesthetised rabbits

Jason P. Kirkness, Hugo K. Christenson*, Sarah R. Garlick, Radha Parikh, Kristina Kairaitis, John R. Wheatley and Terence C. Amis

The obstructive sleep apnoea syndrome (OSA) is a disorder characterised by repetitive closure and re-opening of the upper airway during sleep. Upper airway luminal patency is influenced by a number of factors including: intraluminal air pressure, upper airway dilator muscle activity, surrounding extraluminal tissue pressure, and also surface forces which can potentially act within the liquid layer lining the upper airway. The aim of the present study was to examine the role of upper airway mucosal lining liquid (UAL) surface tension () in the control of upper airway patency. Upper airway opening (P_O) and closing pressures (P_C) were measured in 25 adult male, supine, tracheostomised, mechanically ventilated, anaesthetised (sodium pentabarbitone), New Zealand White rabbits before (control) and after instillation of 0.5 ml of either 0.9 % saline (n = 9) or an exogenous surfactant (n = 16; Exosurf Neonatal) into the pharyngeal airway. The of UAL (0.2 µl) was quantified using the 'pull-off' force technique in which is measured as the force required to separate two curved silica discs bridged by the liquid sample. The of UAL decreased after instillation of surfactant from 54.1 ± 1.7 mN m^-1 (control; mean ± S.E.M.) to 49.2 ± 2.1 mN m^-1 (surfactant; P < 0.04). Compared with control, P_O increased significantly (P < 0.04; paired t test, n = 9) from 6.2 ± 0.9 to 9.6 ± 1.2 cmH₂O with saline, and decreased significantly (P < 0.05, n = 16) from 6.6 ± 0.4 to 5.5 ± 0.6 cmH₂O with surfactant instillation. Findings tended to be similar for P_C. Change in both P_O and P_C showed a strong positive correlation with the change in of UAL (both r > 0.70, P < 0.001). In conclusion, the patency of the upper airway in rabbits is partially influenced by the of UAL. These findings suggest a role for UAL surface properties in the pathophysiology of OSA.

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