Early albumin leakage in pulmonary endothelial monolayers exposed to varying levels of hyperoxia.

We assessed the effect of varying levels of hyperoxia on 14C-albumin flux across bovine pulmonary artery endothelial cell (BPAEC) monolayers. Endothelialized nitrocellulose filters were mounted in Ussing-type chambers which were filled with cell culture medium (M 199). Equimolar amounts of 14C-labeled and unlabeled albumin were added to the "hot" and "cold" chambers, respectively, and the monolayers were exposed to 3 hours of varying levels of oxygen (16%, 30%, 40%, 60%, and 95%). When compared to 16% O2, exposure to hyperoxic gas mixtures of 40% or greater progressively increased albumin permeability across endothelial monolayers within 3 hours to a value 2.5 times higher at 95% O2 compared to 16% O2 (p < 0.001). Hyperoxia-induced permeability increases were prevented by catalase, superoxide dismutase, desferrioxamine, and allopurinol. Our data indicate that hyperoxia induces endothelial permeability changes more rapidly than previously reported even at O2 concentrations as low as 40%.