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Hypothermia-induced ischemic tolerance.

S Nishio1, Z F Chen, M Yunoki

  • 1Department of Neuroscience, University of Virginia, Charlottesville 22908, USA.

Annals of the New York Academy of Sciences
|February 11, 2000
PubMed
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Transient hypothermia conditions the brain, creating delayed ischemic tolerance that protects against cerebral infarction for up to seven days. This neuroprotective effect involves protein synthesis and gene expression.

Area of Science:

  • Neuroscience
  • Cellular Biology

Background:

  • Delayed ischemic tolerance is a phenomenon where the brain becomes resistant to injury after a conditioning stimulus.
  • This tolerance can be induced by various stimuli and lasts for several days.

Purpose of the Study:

  • To investigate transient hypothermia as a conditioning stimulus for inducing delayed ischemic tolerance.
  • To determine the duration and underlying mechanisms of hypothermia-induced ischemic tolerance.

Main Methods:

  • Administering transient hypothermia 6 to 48 hours before inducing focal cerebral ischemia in animal models.
  • Utilizing protein synthesis inhibitors (anisomycin) and in vitro electrophysiological studies on brain slices.

Main Results:

  • Transient hypothermia administered prior to ischemia significantly reduced cerebral infarction.

Related Experiment Videos

  • Hypothermia-induced tolerance persisted for up to 7 days and was blocked by anisomycin, indicating a role for protein synthesis.
  • In vitro studies showed reduced hypoxic damage to synaptic responses in hypothermia-preconditioned brain slices.

    • Conclusions:

    • Transient hypothermia effectively induces delayed ischemic tolerance in the brain parenchyma.
    • The development of this tolerance appears to involve increased gene product expression and protein synthesis.
    • Hypothermia holds potential as a clinical conditioning stimulus to limit ischemic injury.