title: Modeling O₂-dependent effects of nitrite reductase activity in blood and tissue on coupled NO and O₂ transport around arterioles.
abstract: Recent evidence in the literature suggests that tissues play a greater role than blood in reducing nitrite to NO under ischemic or hypoxic conditions. Our previous mathematical model for coupled NO and O(2) transport around an arteriole, modified to include superoxide generation from dysfunctional endothelium, was developed further to include nitrite reductase activity in blood and tissue. Steady-state radial and axial NO and pO(2) profiles in the arteriole and surrounding tissue were simulated for different blood flow rates and arterial blood pO(2) values. The resulting computer simulations demonstrate that nitrite reductase activity in blood is not a very effective mechanism for conserving NO due to the strong scavenging of NO by hemoglobin. In contrast, nitrite reductase activity in tissue is much more effective in increasing NO bioavailability in the vascular wall and contributes progressively more NO as tissue hypoxia becomes more severe.
authors: School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA. dgb28@drexel.edu
authors: Donald G
authors: DG
authors: Buerk
authors: Kenneth A
authors: KA
authors: Barbee
authors: Dov
authors: D
authors: Jaron
mesh_terms: D001160:Arterioles / Q000378:metabolism*; D001692:Biological Transport; D003198:Computer Simulation; D006801:Humans; D008954:Models, Biological; D008962:Models, Theoretical; D009569:Nitric Oxide / Q000378:metabolism*; D009572:Nitrite Reductases / Q000378:metabolism*; D009573:Nitrites / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption; D013481:Superoxides / Q000378:metabolism
chemical_list: D009573:Nitrites; D013481:Superoxides; D009569:Nitric Oxide; D009572:Nitrite Reductases; D010100:Oxygen