Abstract

RBC K loss and cellular dehydration are associated with a variety of normal and abnormal erythrocyte conditions. In some cases (normal RBC aging, pyruvate-kinase-deficient RBCs and irreversibly sickled cells) cation and water changes are related to adenosine triphosphate (ATP) depletion and to increased RBC calcium content. In other disorders, such as hereditary xerocytosis, cation depletion and cellular hydration are not related to altered energy or calcium metabolism. Rather, this condition is thought to be due to a structural membrane defect which is manifested by imbalanced cation leaks (K less greater than Na gain) for which the active cation transport is unable to compensate. None of the disorders described here are associated with known structural membrane alterations. The fact that K loss and cellular dehydration are common to several RBC disorders suggests that this phenomenon may have a direct role in membrane injury. This hypothesis is supported by two separate observations: 1)Formation of irreversible sickled cells in vitro is prevented if K and water loss are inhibited, and these effects are independent of ATP depletion and calcium accumulation; 2) the mean critical hemolytic volume is markedly reduced in K- and water-depleted normal RBCs. RBC dehydration without intracellular cation depletion, however, is not associated with changes in mean critical hemolytic volume. These data thus indicate that K loss may have a direct role in RBC membrane injury. The mechanism by which this occurs and the associated alterations in membrane structure, however, remain to be identified.

View details for PubMedID 531041