Oxygen protects rat brain from ischaemic injury

Neurol Res. 1990 Dec;12(4):219-22. doi: 10.1080/01616412.1990.11758593.

Abstract

Interruption of the oxygen supply to the brain promotes functional and structural damage of the brain, such as oedema and swelling. The most prominent cellular reaction to this type of damage has been found to be trophic or proliferative changes in glial cells. We examined dynamic changes in glial cells adjacent to the infarcted tissue in response to oxygenation. Results showed that astrocyte proliferation was seen more at 3 than at 7 days after middle cerebral artery occlusion, while their numbers with and without oxygenation were almost the same. The proliferation of microglia, however, was seen more with than without oxygenation. However, microglia seem to be able to secrete an angiogenetic factor under hypoxic conditions, and are active in terms of superoxide dismutase (SOD). Cerebral blood flow is directly related to tissue oxygen content and its autoregulatory capacity has been found to be greater as the volume contracts. As a result, we suggest that the application of oxygen-treated microglia to ischaemic tissue could diminish tissue damage, and that the most effective oxygenation can be achieved by the withdrawal of blood and reduction of the intracranial pressure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Edema / etiology
  • Brain Edema / prevention & control
  • Brain Ischemia / etiology
  • Brain Ischemia / prevention & control*
  • Cell Division
  • Cerebral Infarction / blood
  • Cerebral Infarction / complications
  • Cerebral Infarction / pathology
  • Cerebral Infarction / therapy*
  • Glial Fibrillary Acidic Protein / analysis
  • Hypoxia / etiology
  • Hypoxia / prevention & control
  • Neuroglia / chemistry
  • Neuroglia / pathology
  • Oxygen / blood
  • Oxygen / therapeutic use*
  • Partial Pressure
  • Rats
  • Rats, Inbred Strains

Substances

  • Glial Fibrillary Acidic Protein
  • Oxygen