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Asthma: surfactant eliminates the early allergen-induced response

Golden Casket Paediatric Research Laboratory, Mater Medical Research Institute, Brisbane, Queensland, Australia

To the Editor:

In their recent article Babu et al. 1 have just published a remarkable finding in which they have clearly demonstrated how the inhalation of synthetic surfactant abolishes the early allergen-induced response in asthmatics. In interpreting these impressive results, however, they invoke theory based upon oedema at whose liquid-air interface surfactant could exert a "high surface pressure".

In pursuing this approach, the authors appear to have ignored a basic principle of surface physics. Forces derived from surface pressure/tension can only be translated into pressure differences for driving fluid (P) if there is appreciable curvature to the interface as expressed by the Laplace equation, viz:

(001)

where is the surface tension (reciprocating surface pressure) and r₁ and r₂ are radii of curvature in mutually perpendicular planes. Thus, respirologists focus much attention upon surface tension at the alveolar level where curvature is high (r₁=r₂175 µm), P amounting to as much as 8.0 cm water gauge (cm.w.g) if surfactant were not reducing the surface tension of water (=69.9 mN·m^–1). However, at the bronchial level (r₁=1 cm; r₂=), the fluid pressure (P) generated by pure water would be less than 0.07 cm.w.g. Hence, even at its highest surface pressure (0), surfactant could have no physiological effect whatsoever. Surfactant would simply cause the surface contribution to oedema formation (P) to fall from one insignificant level to another.

It would therefore seem more likely that surfactant is acting upon the asthmatic lung by the alternative "barrier" mechanism, referenced by the authors 2, whereby surface-active phospholipid (SAPL) binding by adsorption to bronchial epithelium is "masking" irritant receptors which elicit the bronchoconstrictor reflex. However, this alternative approach now invokes the mechanism of adsorption of SAPL to solid surfaces, which conflicts with a belief, culturally embedded in respirology, that surfactant acts only at liquid-air interfaces. It is interesting that this "belief" also conflicts with the roles of SAPL in nonpulmonary sites in vivo and with vast experience in the physical sciences of surfactants studied at solid surfaces where they often form barriers 3.

Any role of surface tension/pressure by surfactant acting at the liquid-air interface of oedema must surely be a red herring, but it should not detract from a most exciting clinical finding.

References

1. Babu KS, Woodcock DA, Smith SE, Staniforth JA, Holgate ST, Conway JH. Inhaled synthetic surfactant abolishes the early allergen-induced response in asthma. Eur Respir J 2003;21:1046–1049.[Abstract/Free Full Text]
2. Hills BA. Asthma: is there an airway receptor barrier?. Thorax 1996;51:773–776.[Free Full Text]
3. Hills BA. An alternative view of the roles of surfactant and the alveolar model. J Appl Physiol 1999;87:1567–1583.[Abstract/Free Full Text]

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