Hyperoxic Reperfusion After Global Ischemia Decreases Hippocampal Energy Metabolism | Zendy

Erica M. Richards | Zendy; Gary Fiskum | Zendy; Robert E. Rosenthal | Zendy; Irene B. Hopkins | Zendy; Mary C. McKenna | Zendy

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Hyperoxic Reperfusion After Global Ischemia Decreases Hippocampal Energy Metabolism

Author(s) -

Erica M. Richards,

Gary Fiskum,

Robert E. Rosenthal,

Irene B. Hopkins,

Mary C. McKenna

Publication year - 2007

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.106.473967

Subject(s) - medicine , pyruvate dehydrogenase complex , hyperoxia , ischemia , citric acid cycle , glutamate receptor , hippocampal formation , endocrinology , metabolism , reperfusion injury , return of spontaneous circulation , resuscitation , anesthesia , cardiopulmonary resuscitation , biochemistry , biology , lung , enzyme , receptor

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.

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