We have examined the filterability of sickle erythrocytes, using an initial-flow-rate method, to determine whether sufficient hemoglobin S polymer forms at arterial oxygen saturation to adversely affect erythrocyte deformability. The amount of intracellular polymer was calculated as a function of oxygen saturation to estimate the polymerization tendency for each of eight patients with sickle cell anemia (SCA). Progressive reduction of oxygen tension within the arterial range caused a sudden loss of filterability of SCA erythrocytes through 5-μm-diam pores at a critical PO2 between 110 and 190 mmHg. This loss of filterability occurred at a higher PO2 than did morphological sickling, and the critical PO2 correlated significantly (r = 0.844-0.881, P < 0.01) with the polymerization tendency for each patient. Study of density-gradient fractionated cells from four SCA patients indicated that the critical PO2 of dense cells was reached when only a small amount of polymer had formed, indicating the influence of this subpopulation on the results obtained for unfractionated cells. Impairment of erythrocyte filterability at high oxygen saturation (> 90%) suggests that small changes in oxygen saturation within the arterial circulation cause rheological impairment of sickle cells.
CITATION STYLE
Green, M. A., Noguchi, C. T., Keidan, A. J., Marwah, S. S., & Stuart, J. (1988). Polymerization of sickle cell hemoglobin at arterial oxygen saturation impairs erythrocyte deformability. Journal of Clinical Investigation, 81(6), 1669–1674. https://doi.org/10.1172/JCI113504
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