Polymerization of sickle cell hemoglobin at arterial oxygen saturation impairs erythrocyte deformability.
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-micron-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 less than 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 (greater than 90%) suggests that small changes in oxygen saturation within the arterial circulation cause rheological impairment of sickle cells.
Green
M A
MA
Department of Haematology, Medical School, University of Birmingham, United Kingdom.
Noguchi
C T
CT
Keidan
A J
AJ
Marwah
S S
SS
Stuart
J
J
D000755:Anemia, Sickle Cell / Q000097:blood*; D002499:Centrifugation, Density Gradient; D004907:Erythrocyte Deformability; D006451:Hemoglobin, Sickle / Q000378:metabolism*; D006720:Homozygote; D006801:Humans; D010100:Oxygen / Q000097:blood*; D011108:Polymers; D012212:Rheology
D006451:Hemoglobin, Sickle; D011108:Polymers; D010100:Oxygen