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An Integrated Mathematical and Experimental Model for Nitric Oxide uptake by Red Blood Cells

Endothelium‐derived nitric oxide (NO) is a potent vasodilator despite the presence of hemoglobin (Hb) encapsulated in red blood cells (RBC) which has high affinity for scavenging NO (k~ 107 M−1 s−1). NO uptake by RBC‐Hb is reported to be several orders lesser than that of free Hb. Reduced uptake by RBC encapsulated Hb is attributed to several diffusional resistances for NO to react with Hb including extracellular resistance, cell free layer resistance near the vessel wall, resistance in unstirred layer surrounding RBCs and resistance by RBC membrane. The extent of contribution from each diffusional layer towards reduced NO uptake by RBCs is under intense investigation. We developed a novel stirred bioreactor with a headspace to maintain controlled NO concentrations. Using this bioreactor along with an electrochemical NO sensor, we measured the bulk NO concentration in RBC suspensions DI water for various NO concentrations in the bioreactor headspace. We developed a steady state one dimensional mathematical model representing NO biotransport using the data obtained from above experiments to predict NO concentration profile and to determine the role of extracellular diffusional resistance, resistance offered by unstirred layer surrounding RBCs and resistance offered by RBC membrane. This integrated analysis will provide quantitative information about NO_RBC interaction parameters.