Effect of nitroprusside on pulmonary hypertension and lung fluid balance after E. coli endotoxin

Pulmonary edema after Escherichia coli (E. coli) endotoxin administration is characterized by marked pulmonary hypertension adn 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 after E. coli endotoxin 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 (P PA) compared to the endotoxin control group. During NP infusion, cardiac output increased a P PA decreased. We found no difference in QL during NP infusion compared to the control group. After cessation of NP infusion, QL increased, whereas protein clearance (QL x lymph protein content) remained constant. We found no beneficial effect of nitroprusside on transvascular fluid flux and microvascular protein permeability after E coli endotoxin injury.