Pulmonary edema afterEscherichia coli (E. coli)endotoxin administration is characterized by marked pulmonary hypertension and microvascular protein permeability. Conceivably, therapy directed at reducing pulmonary arterial hypertension should improve right ventricular mechanics and potentially may decrease the amount of edema formed. We studied the effect of nitroprusside (NP) on pulmonary hypertension, transvascular fluid filtration rate (reflected in lung lymph flow (QL)) and microvascular protein permeability afterE. coliendotoxin lung injury. Using the unanesthetized sheep lung lymph preparation, we found the initial pulmonary hypertension after endotoxin infusion refractory to NP. One h after endotoxin, NP significantly reduced the pulmonary artery pressure (PPA) compared to the endotoxin control group. During NP infusion, cardiac output increased as PlPAdecreased. We found no difference in QLduring NP infusion compared to the control group. After cessation of NP infusion, QLincreased, whereas protein clearance (QLX lymph protein content) remained constant. We found no beneficial effect of nitroprusside on transvascular fluid flux and microvascular protein permeability afterE. coliendotoxin injury.