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2 Division of Pulmonary and Critical Care Medicine and 3 Department of Pathology, Northwestern University, Chicago 60611; 4 Department of Mathematics, Northeastern Illinois University 60625; 5 Division of Pulmonary and Critical Care Medicine, University of Illinois at Chicago, Chicago, Illinois 60612; and 1 Departamento de Enfermedades Respiratorias, Universidad Católica de Chile, Santiago, Chile
Cardiogenic pulmonary edema results from
increased hydrostatic pressures across the pulmonary circulation. We
studied active Na+ transport and alveolar fluid
reabsorption in isolated perfused rat lungs exposed to increasing
levels of left atrial pressure (LAP; 0-20 cmH2O) for
60 min. Active Na+ transport and fluid reabsorption did
not change when LAP was increased to 5 and 10 cmH2O
compared with that in the control group (0 cmH2O; 0.50 ± 0.02 ml/h). However, alveolar fluid reabsorption decreased by
~50% in rat lungs in which the LAP was raised to 15 cmH2O (0.25 ± 0.03 ml/h). The passive movement of
small solutes (22Na+ and
[3H]mannitol) and large solutes (FITC-albumin) increased
progressively in rats exposed to higher LAP. There was no significant
edema in lungs with a LAP of 15 cmH2O when all
active Na+ transport was inhibited by hypothermia or
amiloride (10
4 M) and ouabain (5 × 104 M). However, when LAP was increased to 20 cmH2O, there was a significant influx of fluid (
0.69 ± 0.10 ml/h), precluding the ability to assess the rate of
fluid reabsorption. In additional studies, LAP was decreased from 15 to
0 cmH2O in the second and third hours of the experimental
protocol, which resulted in normalization of lung permeability to
solutes and alveolar fluid reabsorption. These data suggest that in an
increased LAP model, the changes in clearance and permeability are
transient, reversible, and directly related to high pulmonary
circulation pressures.
active sodium transport; lung edema clearance
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