Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism.

Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. Research Abstract Details 

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Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. Abstract Text:

Erica M Richards,Gary Fiskum,Robert E Rosenthal,Irene Hopkins,Mary C McKenna,

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).

Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. Publishing Authors By Initials

EM Richards,G Fiskum,RE Rosenthal,I Hopkins,MC McKenna,

For similar therapeutics: emergency treatment: resuscitation: respiration, artificial research abstracts see: therapeutics: emergency treatment: resuscitation: respiration, artificial research

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Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Stroke; a journal of cerebral circulation

VOLUME: 38

Page Numbers: 1578-84

Journal Abbreviation:

ISSN: 1524-4628

DAY: 5

MONTH: 04

YEAR: 2007

Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 235266

Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. Keywords Mesh Terms:

KEYWORDS: Respiration, Artificial

MESH TERMS: prevention & control

Chemical & Substance for Abstract: Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. Information

Substance Name: Glutamic Acid

Registry Number: 56-86-0

Grant and Affiliation Information for Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism.

AFFILIATION: Program in Neuroscience, the Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS34152

ACRONYM: NS

MEDLINETA: Stroke

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