Abstract
IN homozygous sickle-cell disease, deoxygenation of red cells causes the polymerization of hemoglobin S and transformation of the intracellular fluid into a viscoelastic gel. This process is most prominent in particularly dense red cells that have a high concentration of hemoglobin S. The membrane of these dense red cells also has elevated viscoelastic moduli,1 , 2 probably as a result of mechanical stresses exerted during sickle–unsickle cycles. Therefore, the densest cells are most rigid and have the greatest effect on resistance3 in blood flow through the microcirculation. Studies of the retina of patients with sickle-cell disease4 and the microcirculation of animals receiving . . .