Abstract-The microvascular pulmonary endothelium barrier is critical in preventing interstitial fluid overflow and deterioration in gas diffusion. The role of endothelium in transporting small solutes in pathological conditions, such as congestive heart failure (CHF), has not been studied. Monitoring of pulmonary gas transfer during saline infusion in CHF was used to probe this issue. Carbon monoxide diffusion (DL CO ), its membrane diffusion (D M ) and capillary blood volume (V C ) subcomponents, and mean right atrial (rap) and mean pulmonary wedge (wpp) pressures after saline or 5% .01 versus 750 mL of saline) and decreased V C (Ϫ9, PϽ0.01 versus 750 mL of saline); aldosterone (Ϫ40%), renin (Ϫ41%), hematocrit (Ϫ3%), rap, and wpp behaved as they did after saline infusion. In controls, responses to both saline amounts were similar to responses in CHF patients regarding aldosterone, renin, hematocrit, rap, and wpp, whereas DL CO , D M , and V C values tended to rise. Hindrance to gas transfer (reduced DL CO and D M ) with salt infusion in CHF, despite an increase in V C and no variations in pulmonary hydrostatic forces, indicates an upregulation in sodium transport from blood to interstitium with interstitial edema. Redistribution of blood from the lungs, facilitating interstitial fluid reabsorption, or sodium uptake from the alveolar lumen by the sodium-glucose cotransport system might underlie the improved alveolar-capillary conductance with glucose. (Hypertension. 1999;34:1202-1207.)Key Words: capillaries Ⅲ epithelium Ⅲ glucose Ⅲ heart failure Ⅲ sodium F or the lung parenchyma to allow gas exchange between blood and gas in the alveoli, a continuous clearance is required of the excess of fluid into the interstitial space and the alveolar lumen. Excessive water accumulation in these compartments is called pulmonary and alveolar edema, respectively. The pulmonary microvascular endothelium and the alveolar epithelium constitute a barrier that is critical for gas exchange and modulation of fluid and solute passage between blood, the interstitial compartment, and alveoli. 1 Despite the substantial progress that has been made in understanding the physiology of the endothelial and epithelial layers in regulating lung fluid balance, further study regarding the local and systemic regulatory factors under pathological conditions is necessary. 1 An imbalance in hydrostatic forces is interpreted as the basic mechanism for volume overload and cardiogenic pulmonary edema. 2 In congestive heart failure (CHF), pulmonary edema may be absent despite elevation of the hydrostatic pressures 3 or may be present even if pressures are normal. 4 Whether altered hemodynamics are the exclusive mechanisms for pulmonary edema in CHF and whether alterations in the capillary endothelium and/or in the alveolar epithelium barrier contribute to changes in salt, water, and gas transfer have been the subjects of only limited research. 3 Cardiogenic anatomic injuries of the alveolar-capillary membrane have been reported in animals and humans. 5,6 ...