“Dewatering” of the lungs at birth

One of the most remarkable events to witness is the very rapid replacement of fluid by air in the normal neonatal lung at birth. Transformation to air breathing is so rapid that it is very difficult to envisage the normal physiological mechanisms for maintaining homeostasis in the air filled lung expelling so much fluid so rapidly—especially when, up to that point, those mechanisms have been shifting fluid in the reverse direction in utero.

Such rapid expulsion of aqueous fluid from porous media are commonly effected in the physical sciences by use of cationic surfactants termed “de-watering” agents.1 They function by chemisorption to the solid surface, reversibly bound by their polar moieties, to impart some degree of hydrophobicity and, hence, water repellency.

It has been suggested1 that, in the normal air filled lung, water repellency imparted by an adsorbed pseudo-cationic surfactant in the form of surface active phospholipid (SAPL), is responsible for alveolar fluid being confined to the “pools” observed2 in the septal corners, and “pits” elsewhere along what is otherwise an apparently fluid free surface. A continuous liquid layer would impair gas exchange.

This concept, however, conflicts with popular respiratory theory3 which, unlike the physical sciences,1restricts the role of surfactant in the lung to the liquid–air interface where it reduces surface tension of the alveolus viewed as a one sided bubble.3 This “bubble” model gains its popularity from the fact that a liquid–air interface must dominate entry of the first breath into a lung initially filled with fluid. Moreover, exogenous surfactant formulated to spread rapidly over liquid–air interfaces is usually successful in rapidly establishing adequate gas exchange in infants afflicted with respiratory distress syndrome.4 However, events occurring some 48 hours later determine the ultimate outcome of “surfactant rescue,”4 weaning …