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Brain Ischemia and Reperfusion Injury

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Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 9))

Abstract

During ischemia, brain injury results from an inadequate supply of substrate (oxygen and glucose) to meet metabolic needs. The most common clinical etiology for cerebral hypoxia is cerebral ischemia or the lack of an adequate blood supply to meet the brain’s metabolic needs. Cerebral ischemia may occur in a variety of clinical settings including head trauma, postsurgical brain swelling, subarachnoid hemorrhage, stroke, and cardiac arrest. Even though ischemia is a recurring theme in each of these clinical settings it is clear from laboratory work that the pathophysiology of brain injury varies with different types of ischemia and therefore requires different therapeutic interventions. We will begin this review with a discussion of blood flow and metabolic changes during ischemia and the role of ion fluxes, ischemia induced release of excitatory amino acids and production of oxygen-derived free radicals in the pathophysiology of ischemic brain injury. We will conclude with a discussion of potential therapeutic options in protecting the brain from ischemic damage.

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© 1989 Springer-Verlag Berlin Heidelberg

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Kirsch, J.R., Helfaer, M.A., Koehler, R.C., Traystman, R.J. (1989). Brain Ischemia and Reperfusion Injury. In: Bihari, D., Holaday, J.W. (eds) Brain Failure. Update in Intensive Care and Emergency Medicine, vol 9. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83929-0_6

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  • DOI: https://doi.org/10.1007/978-3-642-83929-0_6

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-51655-2

  • Online ISBN: 978-3-642-83929-0

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