Neuronal ischemic injury: light microscopy, ultrastructure and biochemistry

A uniform, predictable pattern of cellular abnormalities is seen after complete, irreversible ischemic injury to the central nervous system. This is in contrast to the heterogeneous, multifocal picture which characterizes incomplete ischemia. The range of abnormalities in neuronal soma after an arte...

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Bibliographic Details
Published in:Acta neuropathologica 1978-01, Vol.43 (1-2), p.85-95
Main Authors: Garcia, J H, Lossinsky, A S, Kauffman, F C, Conger, K A
Format: Article
Language:English
Subjects:
Alanine - analysis
Animals
Aspartic Acid - analysis
Brain - blood supply
Brain Chemistry
Brain Death
Cats
Cell Survival
Cerebrovascular Disorders - pathology
Encephalomalacia - pathology
Female
Glutamates - analysis
Glutamine - analysis
Haplorhini
Humans
Ischemia - pathology
Macaca mulatta
Male
Microscopy, Electron
Neurons - ultrastructure
Rats
Time Factors
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Summary:A uniform, predictable pattern of cellular abnormalities is seen after complete, irreversible ischemic injury to the central nervous system. This is in contrast to the heterogeneous, multifocal picture which characterizes incomplete ischemia. The range of abnormalities in neuronal soma after an arterial occlusion changes considerably as a function of time and site. There is no single pattern of neuronal alteration that can be ascribed exclusively to ischemia. Red neurons are a relatively late (about 18 h) indicator of ischemia and are seen only in areas where blood supply is marginal. In addition to depletion of high-energy-phosphate reserves, brain ischemia results in characteristic alterations of amino acid concentrations in the ischemic tissue. Glutamate, glutamine, and aspartate either decrease or remain constant while alanine increases. Proportional decreases in the former three amino acids may be explained by simple dilution due to edema. Increases in alanine relative to glutamate and aspartate may be utilized as a biochemical index of perfusion to various brain regions.
ISSN:0001-6322
1432-0533
DOI:10.1007/BF00685002