A reevaluation of the cause of acute hypercalcemia following intravenous administration of lead acetate
Talmage, R.V.; Vander Wiel, C.J.; Norimatsu, H.
Calcified Tissue Research 26(2): 149-153
1978
ISSN/ISBN: 0008-0594 PMID: 737561 Document Number: 332
The effect of i.v. injection of lead acetate (15 or 30 mg/kg) was studied in young adult male rats. The reaction of Pb with rat plasma to produce colloidal material containing Ca and phosphate was demonstrated in vitro and in vivo. This material could be centrifuged down at 25,000 .times. g from plasma aliquots to which Pb was added or from plasma samples obtained as early as 5 min after i.v. Pb injection. The hypercalcemia and hyperphosphatemia reached their peak rapidly after Pb injection, and even at the higher dose level these lasted less than 6 h. 45Ca and 32P were injected at times varying from 1-8 days prior to Pb administration. Plasma radioactivity levels rose with their stable counterparts without affecting plasma nuclide specific activity. Pb uptake on bone surfaces could be detected within 5 min of injection and continued to accumulate for at least 6 h. Although Pb attaches to bone surfaces, the hypercalcemia and hyperphosphatemia are caused by the direct interaction of Pb with Ca and phosphate in solution in plasma. The formation of the colloidal material lowers ionic Ca and phosphate. In vivo, Ca and phosphate are immediately withdrawn from extravascular sources returning plasma concentrations to their initial value. The source of at least the Ca is believed to be bone. The attachment of Pb to bone surfaces does not in itself release significant amounts of Ca and phosphate into blood.
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