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Cytoprotective Drugs After Subarachnoid Hemorrhage

  • Chapter
Stroke

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 27))

  • 182 Accesses

Abstract

Many mechanisms have been postulated to account for vasospasm following sub­arachnoid hemorrhage (SAH). These include nitric oxide, oxygen-derived free radicals, endothelins, protein kinase C activation, changes in endothelial Ca2 + and K+ fluxes, increases in platelet-activating factor, and loss of smooth muscle phosphatases. Many of these different pathologic systems can be tied together. The excitatory amino acid systems can result in generation of free radicals. The systems that produce reperfusion injury can develop free radicals. Nitric oxide itself can function as a free radical and can increase the production of others. Lipid peroxidation can result in more extracellular glutamate release.

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Authors
  1. T. P. Bleck
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Editors and Affiliations

  1. Neurologische Klinik, Universität Heidelberg, Im Neuenheimer Feld 400, D-69120, Heidelberg, Germany

    Thorsten Steiner  & Werner Hacke  & 

  2. Division of Neurosciences Critical Care, John Hopkins University, Medical School, 600 North Wolfe Str/Meyer 8-140, 21287-7840, Baltimore, MD, USA

    Daniel F. Hanley

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© 1998 Springer-Verlag Berlin Heidelberg

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Bleck, T.P. (1998). Cytoprotective Drugs After Subarachnoid Hemorrhage. In: Steiner, T., Hacke, W., Hanley, D.F. (eds) Stroke. Update in Intensive Care and Emergency Medicine, vol 27. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60264-1_18

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  • DOI: https://doi.org/10.1007/978-3-642-60264-1_18

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-64326-2

  • Online ISBN: 978-3-642-60264-1

  • eBook Packages: Springer Book Archive

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