ALVEOLAR AIR TISSUE INTERFACE AND NUCLEAR-MAGNETIC-RESONANCE BEHAVIOROF NORMAL AND EDEMATOUS LUNGS

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. This signal loss can be measur ed as the difference in NMR signal intensity (difference signal Delta) between a pair of images obtained using temporally symmetric and asym metric 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. Theore tically, the NMR behavior of edematous lungs is expected to differ fro m that of normal nondegassed lungs because alveolar flooding and colla pse are equivalent to partial (regional) degassing. To test this predi ction, we measured Delta 6ms in normal and edematous (oleic acid-injur ed) excised unperfused rat lungs at 5, 10, 20, 30, and 0 (full passive deflation) cm H2O inflation pressure (PL). Lung volume changes were e stimated from NMR lung water density (rho(-)H2O) measurements. In norm al 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. U pon subsequent deflation from 30 to 0 cm H2O PL, Delta 6ms did not var y significantly or decreased. On the basis of our theoretical models, the data could be interpreted as reflecting the loss of alveolar air/t issue interface as a result of alveolar flooding and the relative cont ributions of airspace recruitment and distension to the lung volume ch anges. Histologic and morphometric data obtained from the same lungs s upported this interpretation. Our results suggest that Delta 6ms measu rements can be used to characterize experimental lung injury. Combined measurements of rho(-)H(2)O and Delta 6ms may provide a method for di fferentiating alveolar from interstitial edema and for assessing the r elative roles of airspace recruitment and distension in the lung press ure-volume behavior.