Effects of methylprednisolone on the physical properties of the human red cell.
Rand Pw, Eleanor H. Lacombe, Barker Nd, Kallechey Gl
Abstract
Rand Pw, Eleanor H. Lacombe, Barker Nd, Kallechey Gl
Abstract
Prompted by evidence suggesting preserved red cell deformability in cardiac surgical patients pretreated with pharmacologic dosages of methylprednisolone, we performed in vitro experiments to examine the ability of similar levels of methylprednisolone and hydrocortisone to modify erythrocyte membrane changes produced by metabolic depletion or membrane-active compounds. Variables measured included cell morphology, blood biscosity, membrane deformability, osmotic fragility, red cell cholesterol, and glycolytic intermediates. In incubated samples, methylprednisolone partially prevented the transition of discs to echinocytes, the rise in whole blood viscosity, the decrease in membrane deformability, and the loss of red cell cholesterol which accompany ATP depletion, but it had no apparent effect on red cell glycolysis. The drug also inhibited esterification of cholesterol in cell-free serum. In unimcubated samples to which lysolecithin was added, methylprednisolone partially prevented and reversed morphologic and rheologic responses without affecting membrane cholesterol. Hydrocortisone demonstrated similar properties. Possible mechanisms for these actions are discussed. The concept is advanced that preserved blood fluidity may contribute to the beneficial responses to these drugs in certain clinical conditions.
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Prompted by evidence suggesting preserved red cell deformability in cardiac surgical patients pretreated with pharmacologic dosages of methylprednisolone, we performed in vitro experiments to examine the ability of similar levels of methylprednisolone and hydrocortisone to modify erythrocyte membrane changes produced by metabolic depletion or membrane-active compounds. Variables measured included cell morphology, blood biscosity, membrane deformability, osmotic fragility, red cell cholesterol, and glycolytic intermediates. In incubated samples, methylprednisolone partially prevented the transition of discs to echinocytes, the rise in whole blood viscosity, the decrease in membrane deformability, and the loss of red cell cholesterol which accompany ATP depletion, but it had no apparent effect on red cell glycolysis. The drug also inhibited esterification of cholesterol in cell-free serum. In unimcubated samples to which lysolecithin was added, methylprednisolone partially prevented and reversed morphologic and rheologic responses without affecting membrane cholesterol. Hydrocortisone demonstrated similar properties. Possible mechanisms for these actions are discussed. The concept is advanced that preserved blood fluidity may contribute to the beneficial responses to these drugs in certain clinical conditions.
Key concepts: Echinocyte, Red Cell, Methylprednisolone, Erythrocyte fragility, Red blood cell, Glycolysis, Cholesterol, Hydrocortisone