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The efflux of salt from human red blood cells suspended in isotonic sucrose plus low concentrations of salt, was measured under steadystate conditions. The relationship between the efflux and the log of the salt concentration can be fitted by two straight lines with a sharp inflection point, the steeper slope occurring at concentrations below 0.2 mm NaCl. The determining factor in the rate of efflux is the ionic strength rather than the specific monovalent cations or anions and the effects are completely reversible. With an increase in temperature, the effects of reduced ionic strength are more pronounced and the inflection point is shifted toward higher salt concentrations. An increase in pH leads to an increased efflux at a given ionic strength, but the size of the pH effect is small at low ionic strength. At a given pH, the data can be fitted by a simplified form of the Goldman equation suggesting that with reduction in ionic strength, the permeability remains constant until the inflection point is reached. At that ionic strength, a sharp reversible transition to a new permeability state occurs. The permeability increases with an increase in the external but not the internal pH.The rate of leakage of salts from red blood cells is remarkably increased in cells suspended in a medium in which much of the electrolyte is replaced by nonpenetrating nonelectrolyte of equivalent tonicity. In several of the earlier observations the increased leakiness was inferred from changes in osmotic fragility (1, 2), but in others, salt loss was measured directly by changes in the conductivity of the medium (3, 4) or by chemical analysis for K + (5-7). Because red blood cells are more permeable to anions than to cations by many orders of magnitude, the outflow of salts is preceded by a rapid anion equilibration, primarily an exchange of C 1-for OH-, resulting in acidification of the medium (8, 9). The redistribution of anions presumably follows the Donnan equilibrium, resulting in a large potential difference across the membrane, the magnitude of which can be calculated from the Nernst equation using the chloride ratio (inside to outside concentration) (7). Wilbrandt (4) pointed '7'

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In vitro measurements of membrane and whole cell deformability indicate that erythroid maturation is accompanied by a progressive increase in cellular deformability. Early and intermediate normoblasts cannot be entirely deformed into a micropipette with dimensions like those of the apertures in the basement membrane which separates marrow hematopoietic cords from sinuses. Shape and nuclear rigidity are the most important determinants of rigidity in these immature cells. The marrow reticulocyte, with its distinctive clover-leaf configuration, still manifests significant intrinsic rigidity of its membrane and possibly underlying cytoplasm, which may be important to its normal retention in the bone marrow. However, further maturation is accompanied by a progressive decrease in membrane stiffness and, hence, resistance to traversing the micropipette. These results are interpreted to suggest that cellular deformability may be an important determinant of normal release of maturing erythrocytes from the bone marrow.

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