Skip to main content

Glutamate and Free Fatty Acid Concentrations in Extracellular Vasogenic Edema Fluid

  • Chapter

Abstract

Traumatic or ischemic injury to the brain causes focal tissue necrosis together with an opening of the blood-brain barrier leading to an influx of vasogenic edema into the cerebral parenchyma. Clinical and experimental observations suggest an involvement of chemical factors, or compounds mediating secondary brain damage, such as vasogenic brain edema. Mediators may enhance the primary damage inflicted to the blood brain barrier, induce derangements of the cerebral microcirculation, and cause formation of secondary cytotoxic necrosis, or cell swelling in focal and perifocal areas. Many systems and compounds have been studied in this context2. A great number of reports, including those of ourselves demonstrate glutamate and free fatty acids to exhibit powerful neurotoxic properties. These findings together with the occurrence of glutamate and free fatty acids either in the intra-cellular compartment, or the lipid moiety in vast amounts in normal brain render both substances excellent candidates as mediators of secondary brain damage. Exposure of brain tissue to glutamate by iontophoretic administration to cerebral cortex, or by ventriculo-cisternal perfusion in-vivo was found to induce swelling and destruction of cellular elements, or gross brain edema, respective-ly14,l,9,13.

This is a preview of subscription content, log in via an institution.

Buying options

Chapter
USD   29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD   39.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD   54.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Learn about institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Baethmann A, Oettinger W, Rothenfuszer W, Geiger R: Biochemical aspects of cerebral edema. In: Pathophysiology of Cerebral Energy Metabolism, Mrsulja BB, Rakic L, Klatzo I, Spatz M (Eds): Plenum Press New York 189–209 (1979).

    Chapter  Google Scholar 

  2. Baethmann A, Oettinger W, Rothenfuszer W, Kempski O, Unterberg A, Geiger R: Brain edema factors: Current state with particular reference to plasma constituents and glutamate. In: Brain edema, Pathology, Diagnosis and Therapy”, Cervos-Navarro J, Ferszt R (Eds): Adv Neurol 28. Raven Press New York 171–195 (1980).

    Google Scholar 

  3. Bazan NS, Rodriguez de Turco EB: Membrane lipids in the patho-genesis of brain edema: Phospholipids and arachidonic acids, the earliest membrane components changes at the onset of ischemia. In: Brain Edema, Pathology, Diagnosis and Therapy. Cervos-Navarro J, Ferszt R (Eds): Adv Neurol 28. Raven Press New York 179–205 (1980).

    Google Scholar 

  4. Chan PH, Fishman RA: Brain edema: Induction in cortical slices by polyunsaturated fatty acids. Science 201: 358–360 (1978).

    Article  Google Scholar 

  5. Gazendam J, Go KG, Van Zanten AK: Composition of isolated edema fluid in cold-induced brain edema. J Neurosurg 51: 70–77 (1979).

    Article  Google Scholar 

  6. Go KG, Patberg WR, Teelken AW, Gazendam J: The starling hypothesis of capillary fluid exchange in relation to brain edema. In: Dynamics of Brain Edema. Pappius HM, Feindel W (Eds): Springer Berlin-Heidelberg-New York 63–67 (1976).

    Chapter  Google Scholar 

  7. Harvey JA, McIlwain H: Excitatory acidic aminoacids and the cation content and sodium ionflux of isolated tissues from the brain. Biochem J 108: 269–276 (1968).

    Google Scholar 

  8. Henn FA, Goldstein MN Hamberger A: Uptake of the neurotransmitter candidate glutamate by glia Nature 249: 663–664 (1974).

    Google Scholar 

  9. Kempski O, Baethmann A: Localization of cerebral edema induced by glutamate by measurement of tissue impedance. Proc Internat Conf Electr Bio-Impedance, 113–116 Tokyo (1981).

    Google Scholar 

  10. Kontos HA, Wei EP, Povlishock JT, Dietrich WD, Magiera CJ, Ellis EF: Cerebral arteriolar damage by arachidonic acid and prostaglandin G2. Science 109: 1242–1245 (1980).

    Article  Google Scholar 

  11. Lowry OH, Passonneau JV: A Flexible System of Enzymatic Analysis Academic press New York 184 (1972).

    Google Scholar 

  12. Reulen HJ, Graham R, Spatz M, Klatzo I: Role of pressure gradients and bulk flow in dynamics of vasogenic brain edema. J Neurosurgery 46: 24–35 (1977).

    Article  Google Scholar 

  13. Rothenfuszer W: Die Bedeutung von Glutamat als Hirnödemfaktor. Thesis, München (1982).

    Google Scholar 

  14. Van Harreveld A, Fifkova E: Light-and electronmicroscopic changes in central nervous tissue after electrophoretic injection of glutamate. Experiment Molec Pathology 15: 61–81 (1971).

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1984 Plenum Press, New York

About this chapter

Cite this chapter

Hauff, K.M. et al. (1984). Glutamate and Free Fatty Acid Concentrations in Extracellular Vasogenic Edema Fluid. In: Go, K.G., Baethmann, A. (eds) Recent Progress in the Study and Therapy of Brain Edema. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4616-6_17

Download citation

  • DOI: https://doi.org/10.1007/978-1-4684-4616-6_17

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-4618-0

  • Online ISBN: 978-1-4684-4616-6

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics