Posthypertonic Hemolysis in Sodium Chloride Systems

Human erythrocytes were exposed in vitro to hypertonic NaCl solutions and then to near isotonic media. The resulting posthypertonic hemolysis was studied as a function of hypertonic concentration and of time in the hypertonic medium. Providing that a critical concentration level (∼1.5 M NaCl) is exceeded, posthypertonic hemolysis is proportional both to the duration of exposure to hypertonicity and to the hypertonic concentration. The results have been interpreted in terms of a hypothesis put forward by Söderström (1944), who postulated that influx of salt occurred during the hypertonic phase and that a later reduction of the external concentration caused osmotic hemolysis. A rough calculation suggests that only above an external concentration of 0.65 M NaCl will an influx of salt occur. An analysis of the results in terms of this hypothesis suggested that the permeability of the cells to NaCl increases with increasing external NaCl concentration: The permeability increase was very great in the region of 3 M NaCl. The counter‐current multiplier mechanism for kidney function has been criticised on the ground that red cells may not tolerate the tonicity changes postulated to exist in the kidney. In vitro experiments using slightly worse conditions than are believed to exist in the human kidney showed no significant hemolysis.