Effect of furosemide on fully established low pressure pulmonary edema

It has been shown that furosemide, via nondiuretic vascular effects, reduces pulmonary shunt and lung water during the development of oleic acid permeability edema. We studied this effect in a fully established stable model of oleic acid permeability edema. Sixteen anesthetized mongrel dogs, mechanically ventilated with a FIO2 of 0.5, were studied 24 hr after induction of pulmonary capillary leak by intravenous oleic acid (0.06 cc/kg). After stabilization of pulmonary capillary wedge pressure (PCWP) in the range of 0.5-3 mm Hg, bilateral ureteral ligation was performed. Furosemide (2 mg/kg) was then administered intravenously to eight dogs (treated group). An equivalent volume of saline was given to eight control dogs (control group). Pulmonary artery (PAP) and capillary wedge pressures (PCWP), thermodilution cardiac output (Qt), thermal dye lung water (LW), venous admixture (Qva/Qt), arterial and mixed venous blood gases (PaO2, MVO2) were then measured at hourly intervals for 4 hr. During this period of time, central hemodynamics (PCWP, PAP, Qt) remained stable in both groups. Indices of gas exchange and edema formation (Qva/Qt, LW, PaO2) did not change significantly in either control or treated animals. We conclude that furosemide, previously shown to reduce pulmonary shunt and lung water in the early phase of oleic acid permeability edema, does not have any effect once the pulmonary injury is well-established.