AbstractIncreased pulmonary artery pressures and decreased albumin concentrations were established in dogs, in vivo, by circulatory overload and by plasmapheresis. Each change, occurring singly, would be expected to produce an increase in outward filtration rate. The ultrastructure of the alveolar epithelium after the production of this presumed increase in filtration was evaluated by established morphometric techniques. The extent of extravascular fluid accumulation was assessed by multiple indicator‐dilution studies and by light microscopic analysis. Previous studies from this laboratory (DeFouw and Berendsen, 1979; DeFouw, 1980) define increased alveolar surface densities, increased type I cell vesiculation, and depleted type II cell lamellar body contents after increased filtration had induced septal edema and alveolar flooding in isolated perfused dog lungs. In the present study septal edema and alveolar flooding were not detected. Nor were changes observed in either alveolar epithelial cells or in alveolar configurations. However, there was significant accumulation of extravascular fluid in cuffs around extraalveolar vessels. These results are consistent with the interpretation that the initial stage of cardiodynamic edema formation, namely, peri‐vascular cuffing, is not associated with structural aberrations of the alveoli or their lining epithelial cells, in vivo. Since such changes were detected previously in isolated lungs after development of the final stages of edema, namely, septal fluid accumulation and alveolar flooding, additional studies of septal edema and alveolar flooding in intact animals are necessary to establish functional correlates to ultrastructural aberrations in severely edematous lu