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Demonstrates how nitric oxide induces metabolic hypoxia after transient cerebral ischemia, indicating hyperbaric oxygenation can restore mitochondrial respiration.
Improving tissue oxygenation in stroke is an important treatment strategy. Current clinical treatment options focus on early vessel recanalization to restore blood-flow to the ischemic tissue. Ischemic stimuli have been shown to induce a down regulation in mitochondrial respiratory chain activity in several tissues in the past. This effect was demonstrated for up to 72h and is described as “metabolic hypoxia“. Nitric oxide (NO) and oxygen have antagonistic effects on respiratory chain activity by acting in a competitive, dose dependent and reversible manner on complex IV. The increase of NO following ischemic stimuli could be responsible for this metabolic hypoxia, which augments the ischemic tissue damage.
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Eschenfelder et al. (2006) studied this question.
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