Effect of reducing alveolar surface tension on stress failure in
pulmonary capillaries.
Namba, Yasuo, Sanli S. Kurdak, Zhenxing Fu, Odile Mathieu-Costello,
and John B. West.
Department of Medicine, University of California San Diego, La
Jolla CA 92093-0623
APStracts 2:0326A, 1995.
We have previously shown that when pulmonary capillaries are exposed
to high transmural pressures, stress failure of the blood-gas barrier
occurs. It has been suggested that the surface tension of the
alveolar lining layer may protect against stress failure because at
high transmural pressures, the capillaries bulge into the alveolar
spaces. To test this hypothesis, we abolished the gas-liquid surface
tension of the alveoli by filling rabbit lungs with normal saline.
The lungs were then perfused at capillary transmural pressures of
32.5 or 52.5 cmH2O for 1 min with autologous blood, the blood was
washed out with a saline/dextran mixture (3 min), and the lungs fixed
for electron microscopy with buffered glutaraldehyde, all perfusions
at the same pressure. The frequency of breaks was measured in the
capillary endothelial layer, alveolar epithelial layer, and basement
membranes, and the data compared with those in air-filled lungs at
the same capillary transmural pressure and lung volume. We found that
the frequency of breaks in the endothelium was not significantly
different between air and saline filling, and there were fewer breaks
in the outer boundary of the epithelial cells. By contrast, after
saline filling a larger number of breaks were seen in the inner
boundary of the epithelium. The frequency of disruptions of the inner
boundary of the epithelium was closely correlated with the volume of
edema fluid collected at the trachea during the perfusion. These
breaks in the inner boundary of the epithelium had not previously
been seen in air-filled lungs exposed to the same pressures. The
results suggest that abolishing the surface tension of the alveolar
lining layer removes support from parts of the blood-gas barrier when
the capillaries are subjected to a high transmural pressure, but that
not all portions of the barrier are subjected to the same forces.
Received 3 October 1994; accepted in final form 30 June 1995.
APS Manuscript Number A1017-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.