Electrolyte and acid-base balance during acute loading with rubidium chloride.

Previous studies have shown that administration of rubidium to normal or potassium-depleted rats results in a) metabolic acidosis (1), and b) accumulation of rubidium in muscle tissue where it attains final concentrations considerably higher than that of potassium (2). Since it was found that rubidium was at least as effective as potassium in lowering the plasma CO2 content of potassium-deficient nephrectomized animals (1), it was suggested that administered rubidium, like potassium, probably exchanges with intracellular hydrogen.' In view of these facts it was deemed of interest to obtain information about the simultaneous renal and tissue exchanges of electrolytes during loading with rubidium. Short term balance studies were therefore carried out on rats given 40 mEq. per Kg. of RbCl over two days, and the results compared with those in control animals given an equivalent amount of KC1. The data to be reported show that acute loading resulted in the rapid accumulation of very large amounts of rubidium in tissues with the simultaneous displacement of an almost equal amount of intracellular cation. Approximately half of the estimated cellular content of potassium was excreted in the urine together with a