| Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. | |
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MedLine Citation:
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PMID: 17413048 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND AND PURPOSE: Previous reports indicate that compared with normoxia, 100% ventilatory O(2) during early reperfusion after global cerebral ischemia decreases hippocampal pyruvate dehydrogenase activity and increases neuronal death. However, current standards of care after cardiac arrest encourage the use of 100% O(2) during resuscitation and for an undefined period thereafter. Using a clinically relevant canine cardiac arrest model, in this study we tested the hypothesis that hyperoxic reperfusion decreases hippocampal glucose metabolism and glutamate synthesis. METHODS: After 10 minutes of cardiac arrest, animals were resuscitated and ventilated for 1 hour with 100% O(2) (hyperoxic) or 21% to 30% O(2) (normoxic). At 30 minutes reperfusion, [1-(13)C]glucose was infused, and at 2 hours, brains were rapidly removed and frozen. Extracted metabolites were analyzed by (13)C nuclear magnetic resonance spectroscopy. RESULTS: Compared with nonischemic controls, the hippocampi from hyperoxic animals had elevated levels of unmetabolized (13)C-glucose and decreased incorporation of (13)C into all isotope isomers of glutamate. These findings indicate impaired neuronal metabolism via the pyruvate dehydrogenase pathway for carbon entry into the tricarboxylic acid cycle and impaired glucose metabolism via the astrocytic pyruvate carboxylase pathway. No differences were observed in the cortex, indicating that the hippocampus is more vulnerable to metabolic changes induced by hyperoxic reperfusion. CONCLUSIONS: These results represent the first direct evidence that hyperoxia after cardiac arrest impairs hippocampal oxidative energy metabolism in the brain and challenge the rationale for using excessively high resuscitative ventilatory O(2). |
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Authors:
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Erica M Richards; Gary Fiskum; Robert E Rosenthal; Irene Hopkins; Mary C McKenna |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. Date: 2007-04-05 |
Journal Detail:
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Title: Stroke; a journal of cerebral circulation Volume: 38 ISSN: 1524-4628 ISO Abbreviation: Stroke Publication Date: 2007 May |
Date Detail:
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Created Date: 2007-04-24 Completed Date: 2007-05-15 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 0235266 Medline TA: Stroke Country: United States |
Other Details:
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Languages: eng Pagination: 1578-84 Citation Subset: IM |
Affiliation:
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Program in Neuroscience, the Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Brain Ischemia / etiology, physiopathology* Cardiopulmonary Resuscitation Dogs Energy Metabolism / physiology* Female Glucose / metabolism Glutamic Acid / biosynthesis Heart Arrest / complications, therapy* Hippocampus / metabolism* Oxidative Stress Oxygen Inhalation Therapy / methods* Reperfusion Injury / etiology, physiopathology*, prevention & control Respiration, Artificial |
| Grant Support | |
ID/Acronym/Agency:
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HD16596/HD/NICHD NIH HHS; NS049425/NS/NINDS NIH HHS; NS055450/NS/NINDS NIH HHS; NS34152/NS/NINDS NIH HHS; P01 HD016596-240013/HD/NICHD NIH HHS; R01 NS034152-12/NS/NINDS NIH HHS; U01 NS049425-03/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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50-99-7/Glucose; 56-86-0/Glutamic Acid |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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