A reevaluation of the cause of acute hypercalcemia following intravenous administration of lead acetate.

Abstract

The effect of intravenous (i.v.) injection of lead acetate (15 or 30 mg/kg) was studied in young adult male rats. The reaction of lead with rat plasma to produce colloidal material containing both calcium and phosphate was demonstrated both in vitro and in vivo. This material could be centrifuged down at 25,000 ×g from plasma aliquots to which lead had been added or from plasma samples obtained as early as 5 min after i.v. lead injection. The hypercalcemia and hyperphosphatemia reached their peak rapidly after lead injection, and even at the higher dose level these lasted less than 6 h.45Ca and32P were injected at times varying from 1 to 8 days prior to lead administration. Plasma radioactivity levels rose with their stable counterparts without affecting plasma nuclide specific activity. Lead uptake on bone surfaces could be detected within 5 min of injection, and continued to accumulate for at least 6 h. It is concluded that although lead attaches to bone surfaces, the hypercalcemia and hyperphosphatemia are caused by the direct interaction of lead with calcium and phosphate in solution in plasma. The formation of the colloidal material lowers ionic calcium and phosphate. In vivo, calcium and phosphate are immediately withdrawn from extravascular sources returning plasma concentrations to their initial value. The source of at least the calcium is believed to be bone. The attachment of lead to bone surfaces does not in itself release significant amounts of calcium and phosphate into blood.