Sepsis reduces the threshold hydrostatic pressure necessary for pulmonary edema in baboons.

The threshold hydrostatic pressure necessary to produce pulmonary edema may be lowered by a decrease in plasma colloid oncotic pressure (COP) or an increase in capillary permeability. Sepsis is thought to increase capillary permeability. The object of this report was to assess the effect of sepsis on threshold hydrostatic pressure. In five adult male baboons a Foley catheter was inserted into the left atrium. In 1 week negative COP-pulmonary artery wedge (PAW) gradients were generated by decreasing the PAW above COP in 5-mm-Hg increments from 0 to 15 in random order. At each S-mm-Hg increment intrapulmonary shunt (Qs/Qr) was calculated from blood gases. A Qs/Qr of 15% was considered to be significant. Sepsis was then induced by the continuous infusion of E. coli. The animals then underwent a similar sequence of COP-PAW gradients and the measurements were repeated. At every COP-PAW gradient the QslQt was elevated in the septic (S) period over the QslQr during the nonseptic (NS) period. (0 mm Hg 32.61 2 9.02; S, 12.52 -e 4.90, NS; -5 mm Hg -31.13 f 11.41, S; 13.54 f 4.23, NS (P<O.O2); -10 mm Hg -34.33 f 9.66, S, 16.95 k 8.49, NS (P < 0.02); -15 mm -31.54 f 4.87, S, 26.06 *-9.09, NS). The threshold COP-PAW gradient is raised from -10 in the nonseptic period to 0 in the septic period. Sepsis increases QslQr significantly over the effect of increased hydrostatic pressure alone (linear model (P < 0.001)). Sepsis lowers the hydrostatic pressure necessary to cause pulmonary edema.