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I stand corrected over my description of their model of the alveolus as “dry.” This was a short hand term on my part to distinguish Hills’ theory on which he has published widely from the more traditional theories of how pulmonary surfactant works.
Their letter, however, does not challenge the basic points I made in reluctantly refuting their hypothesis. These were, firstly, that fetal lung liquid can be absorbed before birth—that is, before the establishment of an air–liquid interface and thus before surface forces can act—and secondly, that even in neonates who have intact pulmonary surfactant function, there is total failure of lung liquid removal when sodium ion transport is abolished.3 The latter finding, in particular, must make us question whether surfactant has any role in lung liquid removal at birth.
The authors make the novel suggestion in their letter that the oligolamellar structures of surfactant could be the barrier to diffusion at intercellular junctions—an action which they claim makes the lung epithelium relatively tight and thus enhances its ability to secrete or absorb liquid through generating osmotic forces by ion movement. Before birth the pulmonary epithelium is already “tight” and restricts the passage of molecules the size of sucrose and larger.4 The low permeability is constant during gestation5 and does not decrease (at least in the liquid filled lung) when surfactant appears near term, a finding which argues against this newly proposed function for surfactant.
Measuring permeability in the air filled postnatal lung is difficult, but the evidence suggests that there is a temporary increase in permeability over the first 12 hours after birth (probably as the result of stretch) which then reverts to near fetal permeability levels.6 7 The reason that it takes days to clear fluid from the lungs in respiratory distress syndrome (RDS) even after administration of exogenous surfactant, is because the epithelial barrier has been breached in the early stages of the disease and cannot maintain an osmotic gradient, however hard the Na+“pump” works. Indeed, damage to the pulmonary epithelium in RDS has been shown to occur within two minutes of birth.8 It is the slow healing of the epithelium, hindered by persistent barotrauma and high oxygen tensions, which causes the prolonged recovery from severe surfactant deficient RDS.
The picture included in the author’s letter seems to provide evidence for the traditional theory—that surfactant rests on a very thin alveolar liquid layer and not vice versa. The thickness of this layer measured in vivo by physiological means in the air filled lung, rather than by microscopy, is indeed very small. The mean thickness being calculated at only 0.1– 0.2 microns, indicating that in some areas it will be even thinner.9 10
I accept that these physiological measurements are no more able to settle the arguments about how precisely surfactant is distributed in the alveolus than can microscopy. However, for ion transport and water movement to work, there must be ready access to the apically placed epithelial ion channels by ions in the alveolar liquid—the alveolar liquid would be better placed below any surfactant forms rather than above them. A more detailed discussion of the possible interactions between surfactant and lung liquid movement has been given elsewhere.11
The authors are to be complimented on their thought provoking suggestions, but, ultimately, all hypotheses must be supported by experimental evidence.
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