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Mitochondrial Hyperoxidation After Cerebral Anoxia/Ischemia

Eiphenomenon or Precursor to Residual Damage?

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 428))

Abstract

Ischemia and reperfusion afterward provoke a characteristic series of events which is common among tissues. Many of the changes produced by ischemia are easily measurable with non-invasive optical or electrode probes in intact or isolated tissues. Among these changes are shifts toward reduction of the electron carriers of the mitochodrial respiratory chain, depletion of tissue oxygen, suppression of the tissue’s functional activities and loss of ion homeostasis. Figure 1 is a composite drawing which illustrates some of these typical events in the cerebral cortex of an anesthetized rat.

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© 1997 Springer Science+Business Media New York

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Rosenthal, M., Mumford, P.L., Sick, T.J., Pérez-Pinzón, M.A. (1997). Mitochondrial Hyperoxidation After Cerebral Anoxia/Ischemia. In: Harrison, D.K., Delpy, D.T. (eds) Oxygen Transport to Tissue XIX. Advances in Experimental Medicine and Biology, vol 428. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5399-1_27

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  • DOI: https://doi.org/10.1007/978-1-4615-5399-1_27

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7465-7

  • Online ISBN: 978-1-4615-5399-1

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