It has generally been assumed that movement of fluid between the pulmonary microvasculature and surrounding tissues is governed by a "Starling" balance of hydrostatic and protein osmotic forces similar to that which prevails in the extremities. However, both recent and older observations suggest that the lungs are more resistant to edema formation than most other organs. Several structural aspects of the lung may account for protection of the airspaces from edema formation. The pulmonary microvasculature, which comprises >70% of the pulmonary circulatory bed, appears to be less permeable to fluid and electrolytes than the endothelium of the pulmonary arteries and veins and other microvascular exchange areas. This arrangement may help explain why early edema is confined to the perivascular and peribronchial regions and why lymphatics do not reach the alveoli. Unlike the peripheral vasculature, which is compressed by edema formation, the extra-alveolar vessels remain tethered open by airway distention, even when interstitial pressures rise above those in the vessels. This may also facilitate return of proteins to the circulation. Ultrafiltration of plasma may lower local protein concentrations in the interstitium, thereby slowing further edema formation. Transendothelial reabsorption of fluid may also be altered by vesicular transport.