OXYGEN-RADICAL-MEDIATED PERMEABILITY EDEMA AND VASOCONSTRICTION IN ISOLATED PERFUSED RABBIT LUNGS

Abstract

O2 radicals were implicated in the pathogenesis of permeability pulmonary edema. To determine directly if O2 radicals can cause increased alveolar-capillary membrane (ACM) permeability and low-pressure permeability edema, O2 radicals were chemically produced in the salt perfusates of isolated rabbit lungs. The O2 radicals generated by xanthine oxidase caused protein-rich edema and increases in lung perfusion pressures that were inhibitable by catalase (H2O2 scavenger) or dimethylthiourea (hydroxyl radical scavenger) but not by superoxide dismutase. To determine the effect of O2 radicals on ACM permeability without interference from increased perfusion pressures, papaverine was used to maintain baseline perfusion pressures during O2 radical exposure and ACM integrity was then assessed by evaluating the response of isolated lungs to elevated outflow pressures (10 mm Hg for 10 min). Under these conditions, increased ACM permeability manifested by weight gains and lavage albumin accumulations occurred in lungs treated with xanthine oxidase but not in control lungs. O2 radicals can cause increased ACM permeability and vasoconstriction in isolated lungs.