Compression-induced Brain Edema: Regional Changes of Superoxide Free Radicals in the Development of Vasogenic Edema and Tissue Damage in Intracranial Hypertension

  • N. Hayashi
  • T. Tsubokawa
Conference paper


Intracranial hypertension following severe head injury continues to remain a serious problem affecting morbidity and mortality. The major causes of such a seriously elevated intracranial pressure (ICP) are mainly either vascular engorgement (brain swelling) or brain edema. Engorgement occurs when there is a loss of normal regulation of vascular tone, and brain edema can occur due to an increased vascular permeability [7]. Recent studies have indicated that the oxygen derived free radicals may modify the changes of vascular tone, permeability and cell membrane damage in ischemic injury [1], resulting in brain edema and swelling. Despite this conceptual framework, previous studies have failed to elucidate the precise location, characteristics, and magnitude of free radical-induced alterations of the injured tissue. An accurate understanding of the regional changes in free radicals occurring in intracranial hypertension-injured tissue is important for investigating the mechanisms of brain edema and swelling in the central nervous system. One of the problems in such research is that free radicals are extremely labile and difficult to detect in vivo.


Capillary Pressure Vascular Permeability Brain Edema Intracranial Hypertension Normal Brain Tissue 
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  1. 1.
    Chan PH, Schmidley W, Fishman RA, Longer SM (1984) Brain injury, edema, and vascular permeability induced by oxygen-derived free radicals. Neurology 34:315–320PubMedGoogle Scholar
  2. 2.
    Fantone C, Ward PA (1985) Polymorphonuclear leucocyte mediated cell and tissue injury. Prog. Pathol 16:973–978Google Scholar
  3. 3.
    Fridovich I (1983) Superoxide free radical: an endogenous toxicant. Ann Rev Pharmacol Toxicol 23:239–257CrossRefGoogle Scholar
  4. 4.
    Hayashi N (1990) Photochemical mapping technique for superoxide free radicals, vascular permeability, and metabolism in frozen tissue sections. Jap J Soc Laser Med 11:37–44Google Scholar
  5. 5.
    Hayashi N, Tsubokawa T, Green BA, Watson BD, Prado R (1990) A new mapping study of superoxide free radicals, vascular permeability and energy metabolism in central nervous system. Acta Neurochir (Suppl) 51:31–33Google Scholar
  6. 6.
    Kukreja RC, Kontos HA, Hess MH, Ellis EF (1986) PGH synthetase and lipoxygenase generate superoxide in the presence of NADH or NADPH. Cir. Res 59:612–619Google Scholar
  7. 7.
    Langfitt TW, Tannenbaum HM, Kassell NF (1966) The etiology of acute brain swelling. J Neurosurg 24:47–56PubMedCrossRefGoogle Scholar
  8. 8.
    Nakano M, Sugioka K, Ushijima Y, Goto T (1986) Chemiluminescence probe with cypridin luciferin analog, 2-methyl-6-phenyl-3,7-dihydroimidazo[l,2a]pyrazin-3-one, for estimating the ability of human granulocytes to generate superoxide. Anal Biochem 159:363–369PubMedCrossRefGoogle Scholar
  9. 9.
    Poten U, Ratcheson RA, Salford LG, Siesjo BK (1973) Optimal freezing conditions for cerebral metabolites in rats. J Neurochem 21:1127–1138CrossRefGoogle Scholar
  10. 10.
    Wei EP, Christman CW, Kontos HA, Povlishock JT (1985) Effects of oxygen radicals on cerebral arterioles. Am J Physiol 248:H157–H162PubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1993

Authors and Affiliations

  • N. Hayashi
    • 1
  • T. Tsubokawa
    • 1
  1. 1.Emergency Center and Department of Neurosurgery Nihon UniversityTokyoJapan

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