| Secondary energy failure after cerebral hypoxia-ischemia in the immature rat. | |
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MedLine Citation:
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PMID: 15529009 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Robert C Vannucci; Javad Towfighi; Susan J Vannucci |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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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:
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Created Date: 2004-11-05 Completed Date: 2004-12-03 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8112566 Medline TA: J Cereb Blood Flow Metab Country: United States |
Other Details:
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Languages: eng Pagination: 1090-7 Citation Subset: IM |
Affiliation:
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Department of Pediatrics, The Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Hershey, USA. robert.vannucci@verizon.net |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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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:
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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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