INCREASED PULMONARY VASCULAR-PERMEABILITY AS A CAUSE OF RE-EXPANSION EDEMA IN RABBITS

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Abstract
To study the mechanism(s) underlying re-expansion edema, the concentration of labeled albumin (RISA) was measured in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that were collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/g dry lung) was measured using a 24Na indicator. Results in reexpansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs EVECW (3.41 .+-. SD 1.24 ml/g) and (RISA)/L/(RISA)PL (0.84 .+-. SD 0.15) were significantly increased when compared with normal control lungs (2.25 .+-. 0.41 ml/g and 0.51 .+-. 0.20, respectively). Results in oleic acid edema (5.66 .+-. 2.23 ml/g and 0.84 .+-. 0.23) were similar to re-expansion edema. Apparently, re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.