Document Detail


Energy metabolism and selective neuronal vulnerability following global cerebral ischemia.
MedLine Citation:
PMID:  1407279     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A short period of global ischemia results in the death of selected subpopulations of neurons. Some advances have been made in understanding events which might contribute to the selectivity of this damage but the cellular changes which culminate in neuronal death remain poorly defined. This overview examines the metabolic state of tissue in the post-ischemic period and the relationship of changes to the development of damage in areas containing ischemia-susceptible neurons. During early recirculation there is substantial recovery of ATP, phosphocreatine and related metabolites in all brain regions. However, this recovery does not signal restitution of normal energy metabolism as reductions of the oxidative metabolism of glucose are seen in many areas and may persist for several days. Furthermore, decreases in pyruvate-supported respiration develop in mitochondria from at least one ischemia-susceptible region at times coincident with the earliest histological evidence of ischemia-induced degeneration. These mitochondrial changes could simply be an early marker of irreversible damage but the available evidence is equally consistent with these contributing to the degenerative process and offering a potential site for therapeutic intervention.
Authors:
N R Sims
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Neurochemical research     Volume:  17     ISSN:  0364-3190     ISO Abbreviation:  Neurochem. Res.     Publication Date:  1992 Sep 
Date Detail:
Created Date:  1992-11-02     Completed Date:  1992-11-02     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  7613461     Medline TA:  Neurochem Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  923-31     Citation Subset:  IM    
Affiliation:
Department of Medical Biochemistry, Flinders University of South Australia, Adelaide.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / metabolism
Brain Ischemia / metabolism*,  pathology
Cell Death / physiology
Energy Metabolism / physiology*
Humans
Nerve Degeneration / physiology*
Neurons / pathology*
Reperfusion

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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