BRAIN LEAD LEVELS IN HEMORRHAGIC LEAD ENCEPHALOPATHY

Abstract

Lead (Pb) encephalopathy in the newborn rat is characterized by hemorrhage restricted to the cerebellum. This was produced by giving 7 day old rats 0.5ml 1% ²¹⁰Pb-acetate by gastric tube daily x 7. This resulted on day 14 in significantly higher Pb levels in the cerebellum than cerebrum (10.1 ± 4.0 vs 5.0 ± 1.2μg Pb/gm)(M ± SD). Since red blood cells (RBC) contain much Pb, it was unclear whether the higher cerebellar levels reflected extravasation of RBC or increased capillary permeability to Pb. This was resolved by labelling RBC by prior injection of ⁵⁹Fe and quantitation of RBC trapping in brain. Pb administration resulted in a significant increase in RBC sequestration in the cerebellum (from control levels of 10.1 ± 1.1 to 49.3 ± 27.8μl RBC/gm), but little change in the cerebrum (from 9.5 ± 1.0 to 10.9 ± 1.1μl/gm). This increased retention of RBC accounted for 62.7 ± 24.2% of the Pb in the cerebellum and 29.1 ± 7.9% in the cerebrum. The remaining Pb represented the actual concentration of Pb in cerebellum (3.6 ± 2.4μg/gm) and cerebrum (3.6 ± 0.9μg/gm). Thus, the level of Pb in hemorrhagic regions of the brain proved to be identical to that in unaffected regions. The restriction of hemorrhage to the cerebellum despite the uniform distribution of Pb in the brain indicates that the cerebellar capillaries are particularly vulnerable to the toxic effects of Pb.

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