Background: In a homeostatic setting, fluid intake is necessary for metabolic and physiological processes to function properly. Normal red cells are more resistant to changes in serum osmolality than other cells, remaining viable even when serum osmolality decreases to as low as 190 mOsM from the 270-290 mOsM reference interval. The ability of the membrane to deform/reform during shear provides red cells with great resilience to changes in serum osmolality. Although normal red cells are resistant to hemolysis, the osmolality threshold for aberrant red cells, such as sickle cell blood, is unknown. In compared to normal red cells, the main purpose of this study was to determine the osmolality threshold for sickle cell hemolysis.
Methods: Red cells were produced and exposed to a solution of sodium chloride with varying osmolality ranging from 290 to 65 mOsm, as described in the methods section.
Following incubation, the supernatant and pellets were analysed for haemoglobin (spectrometry) and glycophorin A (GPA) concentrations using western blotting techniques.
Normal red cells have an osmolality threshold of 190 mOsM, but sickle erythrocytes have a 170-mOsM osmolality threshold. Both cells ruptured quickly, forming an S-shaped pattern of "cooperation." At 150 mOsM, complete (100%) hemolysis occurred. When the fluid osmolality lowers to 65 mOsM, the haemoglobin retained in pellets declines to 50% (regular red cells) and 20% (sickle red cells).
Conclusion: Sickle cell erythrocytes are more resistant to changes in serum osmolality than normal red cells. This study investigates how patients with normal and sickle cell disease react to changes in serum osmolality during dehydration and rehydration. Intravenous fluids are frequently used as adjuvant therapy to alleviate discomfort and reduce or stop the sickling process. Regulating electrolytes and fluid volume during acute pain episodes may thereby benefit African Americans, who are disproportionately impacted by sickle cell disease.
Author (S) Details
Victoria M. Richardson
Department of Clinical Laboratory Science, School of Health Sciences, Winston Salem State University, Winston Salem, North Carolina, USA.
M. T. Kay Woollen
Department of Clinical Laboratory Science, School of Health Sciences, Winston Salem State University, Winston Salem, North Carolina, USA.
William A. Anong
Department of Clinical Laboratory Science, School of Health Sciences, Winston Salem State University, Winston Salem, North Carolina, USA and Department of Biology/ Medical Laboratory Science, Morgan State University Baltimore, Maryland, USA.
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