Viscosity of Erythrocytes and Sickle Cell Adhesion

When HbS becomes reoxygenated, the polymers within the RBCs disappear, and the cells eventually return to normal shape. Vasoocclussion is caused by a combination of factors. Repeated assaults on RBCs from sickling and unsickling can lead to cell membrane damage, loss of membrane flexibility, and rearrangement of surface phos-pholipids. Damage to cell membranes can interfere with ion transport, leading to loss of potassium and water. This creates dehydrated, dense sickle cells, and irreversible sickle cells (ISCs). ISCs are the densest cells, and they tend to remain sickled even when oxygenated. Rigid ISCs can become trapped in microvasculature, leading to cell fragmentation and chronic hemolysis, thus contributing to short survival of RBCs. The life span of sickled RBCs is markedly shorter (10-20 days) than that of normal RBCs (100-120 days). As intracellular membrane viscosity of HbS-containing RBCs increases, blood viscosity increases, which further contributes to vasoocclussion.8 There

is also increasing evidence that suggest sickle cells adhere to vascular endothelium. ' The combined effects of decreased RBC deformability, slow transit through microcirculation, and adhesion to vascular endothelium contribute to obstruction of small and sometimes large blood vessels. The resulting local tissue hypoxia can accentuate the pathologic process of SCD.

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