Pulmonary reduction of an intravascular redox polymer

Pulmonary endothelial cells in culture reduce external electron acceptors v ia transplasma membrane electron transport (TPMET). In studying endothelial TPMET in intact lungs, it is difficult to exclude intracellular reduction and reducing agents released by the lung. Therefore, we evaluated the role of endothelial TPMET in the reduction of a cell-impermeant redox polymer, t oluidine blue O polyacrylamide (TBOP+), in intact rat lungs. When added to the perfusate recirculating through the lungs, the venous effluent TBOP+ co ncentration decreased to an equilibrium level reflecting TBOP+ reduction an d autooxidation of its reduced (TBOPH) form. Adding superoxide dismutase (S OD) to the perfusate increased the equilibrium TBOP+ concentration. Kinetic analysis indicated that the SOD effect could be attributed to elimination of the superoxide product of TBOPH autooxidation rather than of superoxide released by the lungs, and experiments with lung-conditioned perfusate excl uded release of other TBOP+ reductants in sufficient quantities to cause si gnificant TBOP+ reduction. Thus the results indicate that TBOP+ reduction i s via TPMET and support the utility of TBOP+ and the kinetic model for inve stigating TPMET mechanisms and their adaptations to physiological and patho physiological stresses in the intact lung.