Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism.
Stroke
; 38(5): 1578-84, 2007 May.
Article
en En
| MEDLINE
| ID: mdl-17413048
ABSTRACT
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).
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Terapia por Inhalación de Oxígeno
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Daño por Reperfusión
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Isquemia Encefálica
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Metabolismo Energético
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Paro Cardíaco
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Hipocampo
Tipo de estudio:
Etiology_studies
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Guideline
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Prognostic_studies
Límite:
Animals
Idioma:
En
Año:
2007
Tipo del documento:
Article