On the mechanism of hyperkalaemia due to hyperosmotic expansion with saline or mannitol.

1. To investigate the mechanism of the hyperkalaemia that results from hyperosmotic infusions of saline or mannitol, nephrectomized dogs received hyperosmotic infusions of sodium chloride or mannitol with various amounts of sodium bicarbonate. Pa,co2 was held constant. Body spaces and mean whole-body intracellular hydrogen ion activity [H+]i were measured with tritiated water, Na3 6Cl, and [14C]5,5-dimethyl-2,4-oxazolidinedione (DMO). 2. The extracellular hydrogen ion activity after infusion varied, but all animals developed intracellular alkalosis ([H+]i-35 nmol/l, SEM± 5, P<O·OOl). There was no net movement of Na+ across cell membranes. There was a significant negative correlation between the changes in extracellular hydrogen ion and that in extracellular potassium concentrations. A greater apparent cellular penetration ofHC03 resulted in less net loss ofK+ from cells (r = 0'69, P<O·Ol). 3. The results suggest that the hyperkalaemia secondary to hyperosmolar infusion of saline or mannitol is not due to extracellular acidosis, but cellular dehydration, altered cell metabolism or altered cell-membrane function may contribute to the leak of K + from cells in these circumstances.