The alveolar air/tissue interface markedly affects the NMR properties of lungs by causing an NMR signal loss as a result of internal (tissue-induced) magnetic field inhomogeneity. The signal loss can be measured as the difference in NMR signal intensity (difference signal delta) between a pair of images obtained using temporally symmetric and asymmetric spin-echo sequences. Previous data indicate that the difference signal measured at an asymmetry time of 6 ms (delta 6ms) is very low in degassed lungs and increases markedly with alveolar opening. Theoretically, the NMR behavior of edematous lungs is expected to differ from that of normal nondegassed lungs because alveolar flooding and collapse are equivalent to partial (regional) degassing. To test this prediction, we measured delta 6ms in normal and edematous (oleic acid-injured) excised unperfused rat lungs at 5, 10, 20, 30, and 0 (full passive deflation) cm H2O inflation pressure (PL). Lung volume changes were estimated from NMR lung water density (pH2O) measurements. In normal lungs, delta 6ms did not vary with PL. In edematous lungs delta 6ms was, as predicted, significantly lower than normal at 5 and 10 cm H2O PL but rose markedly (to about normal) as PL was further increased. Upon subsequent deflation from 30 to 0 cm H2O PL, delta 6ms did not vary significantly or decreased. On the basis of our theoretical models, the data could be interpreted as reflecting the loss of alveolar air/tissue interface as a result of alveolar flooding and the relative contributions of airspace recruitment and distension to the lung volume changes. Histologic and morphometric data obtained from the same lungs supported this interpretation.(ABSTRACT TRUNCATED AT 250 WORDS)