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1 Department of Biomedical Engineering, Marquette University, Milwaukee 53201-1881; Departments of 2 Pulmonary and Critical Care Medicine, 3 Physiology, 5 Anesthesiology, and 6 Pharmacology/Toxicology, Medical College of Wisconsin, Milwaukee 53226; 7 Zablocki Veterans Affairs Medical Center, Department of Veterans Affairs, Milwaukee, Wisconsin 53295; and 4 Department of Chemistry, Polytechnic University, Brooklyn, New York 11201
Pulmonary endothelial cells in culture reduce external electron acceptors via 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, toluidine blue O polyacrylamide (TBOP+), in intact rat lungs. When added to the perfusate recirculating through the lungs, the venous effluent TBOP+ concentration decreased to an equilibrium level reflecting TBOP+ reduction and autooxidation of its reduced (TBOPH) form. Adding superoxide dismutase (SOD) 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 excluded release of other TBOP+ reductants in sufficient quantities to cause significant TBOP+ reduction. Thus the results indicate that TBOP+ reduction is via TPMET and support the utility of TBOP+ and the kinetic model for investigating TPMET mechanisms and their adaptations to physiological and pathophysiological stresses in the intact lung.
lung metabolism; oxidation-reduction; mathematical modeling; superoxide; ascorbate
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