Abstract
Red blood cells (RBCs) capability to deliver oxygen (O2) has been routinely measured by P50. Although this defines the ability of RBCs to carry O2 under equilibrium states, it cannot determine the efficacy of O2 delivery in dynamic blood flow. Here, we developed a microfluidic analytical platform (MAP) that isolates single RBCs for assessing transient changes in their O2 release rate. We found that in vivo (biological) and in vitro (blood storage) aging of RBC could lead to an increase in the O2 release rate, despite a decrease in P50. Rejuvenation of stored RBCs (Day 42), though increased the P50, failed to restore the O2 release rate to basal level (Day 0). The temporal dimension provided at the single-cell level by MAP could shed new insights into the dynamics of O2 delivery in both physiological and pathological conditions.
Highlights
Red blood cells (RBCs) capability to deliver oxygen (O2) has been routinely measured by P50
To quantitatively assess the O2 release rate from single RBCs, we first fitted the experimental data using nonlinear regression, pressure of O2 (PO2) 1⁄4 AeÀKt, where A is the initial PO2 in the microwell (155.3 mmHg), K denotes the decay constant, and t represents time
Our results revealed that microwells with single RBCs showed a significantly larger D50 (1.17 ± 0.52 s) than those without RBCs (0.80 ± 0.29 s) (Fig. 1d)
Summary
Red blood cells (RBCs) capability to deliver oxygen (O2) has been routinely measured by P50. The ability of RBCs to deliver O2 has been routinely characterized solely by their HbO2 affinity (P50), defined as the partial pressure of O2 (PO2) required to saturate Hb to 50% in a thermodynamic equilibrium process[1] This metric, neglects the dynamic release rate of O2 from RBCs, and may be insufficient to assess the efficacy of RBC O2 delivery in the microcirculation. Our motivation for this study is echoed by a recent study that investigated alterations in the O2 release rate of RBCs with varying cytoplasmic diffusivity[11] They have shown that an increase in pathlength or tortuosity of RBCs under engineered and diseased conditions can lead to a decrease in O2 transport. Their measurements failed to isolate single cells from intercellular diffusion, unlike the current study. We confirmed that the P50 value alone does not substantiate how fast RBCs can diffuse O2 even at the bulk level
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