Document Detail


Secondary energy failure after cerebral hypoxia-ischemia in the immature rat.
MedLine Citation:
PMID:  15529009     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A delayed or secondary energy failure occurs during recovery from perinatal cerebral hypoxia-ischemia. The question remains as to whether the energy failure causes or accentuates the ultimate brain damage or is a consequence of cell death. To resolve the issue, 7-day postnatal rats underwent unilateral common carotid artery occlusion followed thereafter by systemic hypoxia with 8% oxygen for 2.5 hours. During recovery, the brains were quick frozen and individually processed for histology and the measurements of 1) high-energy phosphate reserves and 2) neuronal (MAP-2, SNAP-25) and glial (GFAP) proteins. Phosphocreatine (PCr) and ATP, initially depleted during hypoxia-ischemia, were partially restored during the first 18 hours of recovery, with secondary depletions at 24 and 48 hours. During the initial recovery phase (6 to 18 hours), there was a significant correlation between PCr and the histology score (0 to 3), but not for ATP. During the late recovery phase, there was a highly significant correlation between all measured metabolites and the damage score. Significant correlation also exhibited between the neuronal protein markers, MAP-2 and SNAP-25, and PCr as well as the sum of PCr and Cr at both phases of recovery. No correlation existed between the high-energy reserves and the glial protein marker, GFAP. The close correspondence of PCr to histologic brain damage and the loss of MAP-2 and SNAP-25 during both the early and late recovery intervals suggest evolving cellular destruction as the primary event, which precedes and leads to the secondary energy failure.
Authors:
Robert C Vannucci; Javad Towfighi; Susan J Vannucci
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism     Volume:  24     ISSN:  0271-678X     ISO Abbreviation:  J. Cereb. Blood Flow Metab.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-11-05     Completed Date:  2004-12-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8112566     Medline TA:  J Cereb Blood Flow Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1090-7     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, The Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Hershey, USA. robert.vannucci@verizon.net
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Age Factors
Animals
Biological Markers
Brain / growth & development,  metabolism*
Creatine / metabolism
Energy Metabolism / physiology*
Female
Hypoxia-Ischemia, Brain / metabolism*
Phosphocreatine / metabolism
Pregnancy
Rats
Rats, Wistar
Chemical
Reg. No./Substance:
0/Biological Markers; 56-65-5/Adenosine Triphosphate; 57-00-1/Creatine; 67-07-2/Phosphocreatine

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


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