In 25 rabbits anesthetized with pentobarbital sodium and paralyzed with succinylcholine chloride, we investigated the contributions of four factors that might cause the decreased static lung compliance found in oleic acid-induced pulmonary edema: 1) foam, 2) accumulation of fluid in the interstitial spaces, 3) loss of ventilatable units secondary to alveolar flooding, and 4) increased surface tension. Pulmonary edema, reflected by a 115% increase in mean post-mortem extravascular bloodless lung water content, decreased compliance 47% and tripled alveolar-arterial PO2 difference. Removing foam by degassing did not affect compliance measurements. Filling the lungs with saline caused similar changes in control and edematous animals. Because the 38% decrease in functional residual capacity was largely attributable to water accumulation, we concluded that loss of ventilatable units accounted for virtually all the decreased static lung compliance. The role of increased surface tension could not be determined directly but was considered relatively less important.