Afflicting 10% of all premature infants, respiratory distress syndrome
(RDS) results from a lack of pulmonary surfactant, a molecular substance
that helps the lung's alveoli (air sacs) do their job of extracting
carbon dioxide from the blood and replacing it with oxygen. The surfactant
prevents the lung's alveoli from collapsing and helps keep them properly
inflated by reducing their surface tension. The absence of surfactant
prevents the alveoli from functioning properly.
In an in-vitro study that may improve treatment of this sometimes
fatal condition, UC-Santa Barbara researchers (Joseph Zasadzinski, 805-893-4769,
gorilla@engineering.ucsb.edu) measured the viscosity in single-molecule
layers of human lung surfactant lipids similar to those used to treat
premature infants with RDS. The viscosity of the single-molecule layer
determines how quickly the lipids spread over the surface of an air
sac.
The researchers found that the single-molecule layers consisted of
islands of two-dimensional lipid crystals (a solid-like sheet of lipids
arranged in a repeating pattern) floating in a continuous sea of lipids
in a more liquid-like state. The relative fractions of area taken up
by crystals and liquids change during the breathing cycle, as inhalation
and exhalation changes the amount of surface area on which the surfactant
can spread.
The researchers found that the viscosity of the single-molecule layer
depends greatly on this relative fraction of crystals and liquids. Below
a critical fraction of crystals, the molecule layer behaves like a liquid,
with a low viscosity and low resistance to spreading. However, as a
critical fraction of crystals is attained, the viscosity changes abruptly
and the single-molecule layer becomes completely rigid and immobile.
Changing the lipid composition can alter the fraction of crystals in
the molecule layer, so it is possible to engineer the surfactant to
have the proper viscosity. The researchers believe that the rapid transition
from liquid to almost rigid is important to keeping the alveoli open
at the end of exhalation, when surface tension forces would like to
empty them completely. These findings should help researchers formulate
better replacement surfactants for treatment of premature infants with
RDS. (Ding et
al., Physical Review Letters, 22 April 2002.)