Cardiogenic pulmonary edema results from increased hydrostatic pressures ac
ross the pulmonary circulation. We studied active Na+ transport and alveola
r fluid reabsorption in isolated perfused rat lungs exposed to increasing l
evels of left atrial pressure (LAP; 0-20 CMH2O) for 60 min. Active Na+ tran
sport and fluid reabsorption did not change when LAP was increased to 5 and
10 CMH2O compared with that in the control group (0 cmH(2)O; 0.50 +/- 0.02
ml/h). However, alveolar fluid reabsorption decreased by similar to 50% in
rat lungs in which the LAP was raised to 15 cmH(2)O (0.25 +/-0.03 ml/h). T
he passive movement of small solutes (Na-22(+) and [H-3] mannitol) and larg
e solutes (FITC-albumin) increased progressively in rats exposed to higher
LAP. There was no significant edema in lungs with a LAP of 15 cmH(2)O when
all active Na+ transport was inhibited by hypothermia or amiloride (10(-4)
M) and ouabain (5 x 10(-4) M). However, when LAP was increased to 20 cmH(2)
O, 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 studie
s, LAP was decreased from 15 to 0 cmH(2)O in the second and third hours of
the experimental protocol, which resulted in normalization of lung permeabi
lity to solutes and alveolar fluid reabsorption. These data suggest that in
an increased LAP model, the changes in clearance and permeability are tran
sient, reversible and directly related to high pulmonary circulation pressu
red.