Transvascular pulmonary fluid transport can be altered by either changing the permeability-surface areas (PS) of the exchange barrier or by changing the overall plasma to interstitial fluid driving force. I am currently investigating the effects of altering either the driving force or capillary surface areas on net fluid movement in the lung. Experiments have been completed in which pulmonary microvascular pressure was elevated in stages by inflating a balloon in the left atrium of unanesthetized sheep. The following parameters were measured: pulmonary artery pressure, left atrial pressure, plasma and lymph colloid osmotic pressure and concentration, the concentrations of eight plasma and lymph protein fractions, lung lymph flow, blood gases, cardiac output and tracer estimates of water PS, urea PS, and extravascular lung water. Experiments are currently underway that probe the effects of isotonic and hypotonic volume loading on transvascular fluid and protein exchange. A mathematical model, based on an equivalent pore analog of the capillary barrier, is being applied to the data. The model-predicted interstitial water volume and lymph protein concentrations are being compared with measured values throughout the transient period. If agreement with experimental data is good the model will be used to predict conditions which may lead to lung edema and, in addition, can be used to predict the rate at which water accumulates in the lungs.