Lead encephalopathy in neonatal Long-Evans rats: morphologic studies.

Lead encephalopathy was produced in neonatal Long-Evans rats by administering daily doses of lead acetate (600 milligrams of lead acetate/kilogram of body weight) through an esophageal catheter. Experimental rat pups showed behavioral changes, failed to gain weight at the same rate as controls, developed a paraplegia and died by 15 days of age. Lead analysis showed very high blood and tissue lead levels. Sequential histopathologic changes were studied in the cerebellum with observations also made in the choroid plexus, cerebral cortex and corpus striatum. Emphasis was placed on the cerebellum because this region of the brain was most severely altered. Petechial hemorrhages were evident in the cerebellum at three days and two days later the hemorrhagic lesions were almost confluent. The molecular and Purkinje cell layers were most extensively damaged by the hemorrhage. At eight, nine and ten days hemorrhages were fewer and massive amounts of edema fluid accumulated in the internal granular layer. Vascular anomalies of developing lead poisoned rats were examined with electron microscopy and with Golgi preparations. The evidence indicates that growing capillaries are the primary structure of the central nervous system (CNS) damaged by lead intoxication. The endothelial bud (or angioblast) appears to be a structure sensitive to lead poisoning and the encephalopathy probably results from the death of many of these buds.