Isolated brain capillaries: A model for the study of lead encephalopathy

Gary W. Goldstein; Jerry S. Wolinsky; Judit Csejtey

doi:10.1002/ana.410010306

Isolated brain capillaries: A model for the study of lead encephalopathy

Gary W. Goldstein, Jerry S. Wolinsky, Judit Csejtey

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33 Scopus citations

Abstract

The reaction of capillaries isolated from rat brain to incubation with 10⁻⁴ M lead nitrate was investigated. Dense inclusions, probably containing lead, were found by electron microscopy inside most of the endothelial cell mitochondria. The steady‐state uptake of calcium by these cells was tripled after the exposure to lead. This increase may have been due in part to inhibition of active calcium efflux, since the adenosine triphosphate–dependent uptake of calcium by membranes prepared from the capillaries was abolished by 10⁻⁵ M Pb(NO₃)₂. In contrast, active uptake of potassium by the intact cells was not altered by lead. These results suggest that alterations in the calcium homeostasis of brain endothelial cells induced by the accumulation of lead may underlie the pathogenesis of brain edema in lead poisoning.

Original language	English (US)
Pages (from-to)	235-239
Number of pages	5
Journal	Annals of neurology
Volume	1
Issue number	3
DOIs	https://doi.org/10.1002/ana.410010306
State	Published - Mar 1977
Externally published	Yes

ASJC Scopus subject areas

Neurology
Clinical Neurology

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title = "Isolated brain capillaries: A model for the study of lead encephalopathy",

abstract = "The reaction of capillaries isolated from rat brain to incubation with 10−4 M lead nitrate was investigated. Dense inclusions, probably containing lead, were found by electron microscopy inside most of the endothelial cell mitochondria. The steady‐state uptake of calcium by these cells was tripled after the exposure to lead. This increase may have been due in part to inhibition of active calcium efflux, since the adenosine triphosphate–dependent uptake of calcium by membranes prepared from the capillaries was abolished by 10−5 M Pb(NO3)2. In contrast, active uptake of potassium by the intact cells was not altered by lead. These results suggest that alterations in the calcium homeostasis of brain endothelial cells induced by the accumulation of lead may underlie the pathogenesis of brain edema in lead poisoning.",

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AU - Goldstein, Gary W.

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AB - The reaction of capillaries isolated from rat brain to incubation with 10−4 M lead nitrate was investigated. Dense inclusions, probably containing lead, were found by electron microscopy inside most of the endothelial cell mitochondria. The steady‐state uptake of calcium by these cells was tripled after the exposure to lead. This increase may have been due in part to inhibition of active calcium efflux, since the adenosine triphosphate–dependent uptake of calcium by membranes prepared from the capillaries was abolished by 10−5 M Pb(NO3)2. In contrast, active uptake of potassium by the intact cells was not altered by lead. These results suggest that alterations in the calcium homeostasis of brain endothelial cells induced by the accumulation of lead may underlie the pathogenesis of brain edema in lead poisoning.

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Isolated brain capillaries: A model for the study of lead encephalopathy

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