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The Contribution of Secondary Mediators to the Etiology and Pathophysiology of Brain Oedema: Studies Using a Feline Infusion Oedema Model

  • Ian R. Whittle
  • I. R. Piper
  • J. D. Miller
Conference paper
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 51)

Summary

Secondary mediator compounds are postulated to have a role in vasogenic oedematogenesis. They may also cause focal brain dysfunction due to their neuronal, axonal and glial modulating properties. Using the feline model of infusion brain oedema the effects of right frontal intracerebral infusion (200 μl/hr for 3 hrs) of saline, bradykinin (10−4 to 10−6M), arachidonic acid (10−2 to 10−3M), 20% protein and four human glioma cyst fluids were evaluated. Somatosensory evoked potentials (SSEP), motor evoked potentials (MEPs), rCBF and rCBF CO2 reactivity (Hydrogen clearance), ICP, craniospinal compliance, local brain tissue water content (microgravimety), brain histology and BBB function (Evans Blue 2%) were measured. Brain water content increased locally from 69% to 79%, ICP increased (by mean 14 mmHg) and compliance decreased (mean 70%) and there were the histological features of brain oedema with all infusates. BBB opening occurred with Bradykinin (+), arachidonic acid (+ +), 20% protein (+ + +) and glioma cyst fluid (4+). Polymorphic and macrophage infiltrates were seen with all infusions but rCBF and MEPs remained normal. SSEPs changed with high dose bradykinin and some glioma cyst infusates whilst CBF CO2 reactivity was locally impaired by all infusates except saline and arachidonic acid. This study suggests that certain compounds in brain oedema fluid could mediate local brain dysfunction.

Keywords

Arachidonic Acid Brain Oedema Evans Blue Brain Water Content Vasogenic Brain Oedema 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • Ian R. Whittle
    • 2
  • I. R. Piper
    • 1
  • J. D. Miller
    • 1
  1. 1.University Department of Clinical NeurosciencesWestern General HospitalEdingburghScotland
  2. 2.Department of Clinical NeurosciencesWestern General HospitalEdingburghScotland

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