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[Neuroprotection. Models and basic principles]

O S Kempski1

  • 1Institut für Neurochirurgische Pathophysiologie der Johannes Gutenberg-Universität Mainz.

Der Anaesthesist
|November 1, 1994
PubMed
Summary

Brain damage from ischemia and reperfusion involves excitotoxins like glutamate, acidosis, and free radicals. Combining therapies such as glutamate antagonists and free radical scavengers can improve outcomes.

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Area of Science:

  • Neuroscience
  • Pathophysiology
  • Pharmacology

Context:

  • Ischemia and reperfusion (I/R) injury are significant causes of brain damage.
  • Secondary damage mechanisms include excitotoxicity, acidosis, free radicals, and microcirculatory disturbances.
  • Understanding these mechanisms is crucial for developing effective treatments.

Purpose:

  • To review recently identified pathophysiologic mechanisms of brain damage during I/R.
  • To discuss novel therapeutic strategies based on these mechanisms.
  • To highlight the potential of combined therapeutic approaches.

Summary:

  • Key mediators of secondary brain damage in I/R include glutamate excitotoxicity, severe tissue acidosis (pH 6.0), free radical generation during reperfusion, and microcirculatory impairment.
  • Glutamate, an excitatory neurotransmitter, becomes neurotoxic under limited energy supply, leading to neuronal dysfunction and death.
  • Free radicals damage lipids in cell membranes and myelin, while acidosis disrupts neuronal functions and causes glial swelling.

Impact:

  • Therapeutic strategies include glutamate antagonists, acidosis normalization, diuretics for glial swelling, free radical scavengers (e.g., 21-aminosteroids, allopurinol), and hypothermia.
  • Ensuring rapid reperfusion via hypervolemic hemodilution and blood pressure stabilization is vital for resuscitation and early stroke management.
  • Combining multiple therapeutic principles is expected to significantly improve patient outcomes in I/R injury.

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