Figure 7.
Reduced deformability of AS mouse RBCs under hypoxia is accentuated by hyperosmolality and/or acidosis. (A) Human SCD sample to illustrate typical Oxygenscan profile and readouts. PoS is calculated as the downward inflection point at which there is a >5% drop in the EI Max. (B) Whole blood samples demonstrating no change in deformability in AA or AS mice with deoxygenation. In SS mice, the baseline EI Max was lower, indicative of reduced RBC deformability even under normoxic conditions. During progressive hypoxia, only SS RBCs underwent sickling. (C) Effect of acidosis. At a pH of 6.9, a barely discernible PoS was observed in AS mice, with a more exaggerated profile in SS. (D) Effect of hyperosmolality (460 mOsm/kg). Baseline EI Max was diminished in all genotypes, presumably due to osmotically induced RBC dehydration. Thereafter, reversible sickling was evident in both AS and SS samples. (E) Effect of acidosis (pH 6.9) and hyperosmolality (460 mOsm/kg). The EI Max was lower in AS than in AA, although a clearly reversible component of the EI indicative of reversible sickling was apparent. Notably, the Oxygenscan profile in AA samples in hypertonic conditions also demonstrated a late downward inflection of the EI Max during deoxygenation. Given the impossibility that this is due to RBC sickling, it presumably reflects a sudden deformability change in RBC membranes that unlike sickling, appears to be irreversible, because no rebound in EI is seen during reoxygenation. Panels B-E contain data from 4 AA, 6 AS, and 2 SS mice, including both genders. EI Max, maximum elonagtion index; EI Min, mimimum elongation index.

Reduced deformability of AS mouse RBCs under hypoxia is accentuated by hyperosmolality and/or acidosis. (A) Human SCD sample to illustrate typical Oxygenscan profile and readouts. PoS is calculated as the downward inflection point at which there is a >5% drop in the EI Max. (B) Whole blood samples demonstrating no change in deformability in AA or AS mice with deoxygenation. In SS mice, the baseline EI Max was lower, indicative of reduced RBC deformability even under normoxic conditions. During progressive hypoxia, only SS RBCs underwent sickling. (C) Effect of acidosis. At a pH of 6.9, a barely discernible PoS was observed in AS mice, with a more exaggerated profile in SS. (D) Effect of hyperosmolality (460 mOsm/kg). Baseline EI Max was diminished in all genotypes, presumably due to osmotically induced RBC dehydration. Thereafter, reversible sickling was evident in both AS and SS samples. (E) Effect of acidosis (pH 6.9) and hyperosmolality (460 mOsm/kg). The EI Max was lower in AS than in AA, although a clearly reversible component of the EI indicative of reversible sickling was apparent. Notably, the Oxygenscan profile in AA samples in hypertonic conditions also demonstrated a late downward inflection of the EI Max during deoxygenation. Given the impossibility that this is due to RBC sickling, it presumably reflects a sudden deformability change in RBC membranes that unlike sickling, appears to be irreversible, because no rebound in EI is seen during reoxygenation. Panels B-E contain data from 4 AA, 6 AS, and 2 SS mice, including both genders. EI Max, maximum elonagtion index; EI Min, mimimum elongation index.

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