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Lung Fluid Exchange after Uneven Pulmonary Artery Obstruction in Sheep

We studied steady state transvascular fluid and protein exchange after uneven obstruction of the pulmonary arteries. In anesthetized sheep, ventilated by positive pressure, we measured pulmonary artery and left atrial pressures, cardiac output, lung lymph flow, and lymph/plasma protein ratios. We calculated pulmonary vascular resistance. In 16 sheep we obstructed the pulmonary arteries with various microemboli or balloons in lobar arteries until pulmonary vascular resistance was 2-3 times baseline. In every experiment, lung lymph flow increased as pulmonary vascular resistance increased. The lymph/plasma protein ratio did not change. In four sheep, we increased left atrial pressure by balloon obstruction of the mitral orifice. Pulmonary artery pressure increased as much as in the embolization experiments and lymph flow increased but the lymph/plasma protein ratio decreased, meaning that the increased fluid and protein flux after embolization cannot be due to high pulmonary artery or pulmonary venous outflow pressures alone. In four sheep we compared obstruction of the lower lobe pulmonary arteries by balloons with that of upper lobe pulmonary arteries. Lower lobe arterial obstruction caused the lymph flow which drains predominantly from the lower lobes to decrease whereas upper lobe artery obstruction increased lymph flow. This means that the increased fluid and protein flux occurred mainly in the open, perfused portion of the microvascular bed. The mechanism of the increased fluid filtration and protein permeability may be related to high vascular pressure and high linear blood flow velocity through a markedly restricted microvascular bed, although release of substances that affect endothelial permeability is not ruled out.