The movement of fluid and solute between the vascular, interstitial, cellular and alveolar compartments in response to hydrostatic pressure and osmotic alterations in the pulmonary blood is under study in isolated perfused and weight monitored lungs and in the intact anesthetized dog. These movements are quantified by nonequilibrium thermodynamics in terms of four coefficients relating fluxes to driving forces across the endothelial and epithelial barriers: filtration coefficient of volumetric flow, and permeability, osmotic reflection and solvent drag reflection coefficients of the solute with respect to the barrier. The filtration coefficient is measured by the lung weight transient response to changes in hydrostatic pressure or solute concentrations. The osmotic reflection coefficient is measured by the weight transient response to permeant solute or by chemical analysis of background dilution of effluent blood samples in response to bolus injection of hypertonic solutions. The permeability coefficient is determined by upslope analysis of multiple indicator dilution curves measured in effluent blood samples in either preparation. The solvent drag reflection coefficient is equated to the osmotic reflection coefficient on theoretical grounds (Onsager reciprocity). These coefficients will be determined for a variety of ions and neutral molecules with varied oil:water distribution coefficients. The effect of decreased temperature (which decreases permeability and reflection coefficients of lipophilic molecules) on gas exchanges will be determined. The effects of stiffening of the red cells on their transit through the lungs will be investigated. The modifiability of the barrier characteristics will be correlated with anatomical changes. The metabolic and transport activities of the intact barriers and of the cellular constituents will be studied both in vivo and in vitro in isolated systems. The factors determining the appearance of pulmonary edema in the isolated perfused preparation will be investigated and the hypothesis tested that small solutes as well as the conventional Starling factors play a role in the control of the extravascular lung water.