Potassium repletion fails to interfere with reduction of serum lithium by sodium polystyrene sulfonate in mice.

Abstract

Previous studies have shown that oral sodium polystyrene sulfonate (SPS) lowers serum lithium concentrations after acute and chronic toxic lithium exposures. Because hypokalemia may represent a deterrent to the clinical use of SPS for lithium intoxication, this study was designed to determine whether potassium (K+) repletion interferes with the effect of SPS on serum lithium. 168 male, CD-1 mice were given lithium chloride (LiCl) (250 mg/kg) by gavage at time 0. Half of the mice were then given SPS (5 g/kg/dose) and half an equivalent volume of water by gavage at times 20 and 40 minutes. Half of each of these subgroups was then given potassium chloride (KCl) (3 mmol/kg) intraperitoneally and half an equivalent volume of normal saline. The animals were then sacrificed at one, two, four, and eight hours after lithium administration and the sera were analyzed for lithium and K+ by atomic absorption spectrophotometry. The groups were compared with analysis of variance. The SPS lowered both lithium and K+ concentrations (ps < or = 0.0001). The KCl treatment was associated with transiently increased K+ concentrations (p < 0.0001) and with mildly elevated lithium concentrations when compared with the results of the animals not treated with KCl (p = 0.0016). The KCl treatment-associated increase in lithium concentration occurred both in the animals treated with water and in those treated with SPS. Potassium repletion did not interfere with the ability of SPS to lower serum lithium concentration in animals experimentally poisoned with lithium.