Document Detail

Is post-hypoxic-ischemic cell damage associated with excessive ATP consumption rather than a failure of ATP production?
MedLine Citation:
PMID:  9116409     Owner:  NLM     Status:  MEDLINE    
Secondary cell damage after ATP depletion due to hypoxia or ischemia is clinically important because it correlates with residual effects; post-hypoxic-ischemic fits can be associated with later cerebral palsy. The mechanisms involved in delayed secondary cell damage are not clear, possibly because extensive relevant evidence is often fragmented. However, a sequence of changes can be suggested; this cross-linked sequence is tentatively outlined in this review. The outline suggests explanations for otherwise ill-understood clinical disturbances such as the loss of inhibitory control in damaged cells and the well documented reduction of cellular ATP. Loss of control may be due to reduced synthesis of control proteins and the reduced ATP concentration may be due to increased energy consumption.
R A Harkness
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Acta paediatrica (Oslo, Norway : 1992)     Volume:  86     ISSN:  0803-5253     ISO Abbreviation:  Acta Paediatr.     Publication Date:  1997 Jan 
Date Detail:
Created Date:  1997-04-18     Completed Date:  1997-04-18     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9205968     Medline TA:  Acta Paediatr     Country:  NORWAY    
Other Details:
Languages:  eng     Pagination:  1-5     Citation Subset:  IM    
Pediatrisk Forskningsinstitutt, Universitetet i Oslo, Norway.
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MeSH Terms
Adenosine Triphosphate / metabolism*
Brain Chemistry
Brain Ischemia / complications,  metabolism*
Cell Hypoxia / physiology
Cerebral Palsy / etiology
Heat-Shock Proteins / physiology
Hypoxia, Brain / complications,  metabolism*
Time Factors
Reg. No./Substance:
0/Heat-Shock Proteins; 56-65-5/Adenosine Triphosphate

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