Cerebral blood flow does not mediate the effect of brain temperature on recovery of extracellular potassium ion activity after transient focal ischemia in the rat

Thomas J. Sick, Ruixia Tang, Miguel A. Pérez-Pinzón

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Temperature plays an important role in determining outcome following both global and focal brain ischemia. After focal ischemia, the degree of infarction decreases with mild hypothermia and increases with mild hyperthermia. In this study, brain extracellular potassium ion activity and local cerebral blood flow were measured in cerebral cortex during 60 min of middle cerebral artery occlusion and 60 min of re-perfusion. Brain temperature was maintained at 32-34°C (mild hypothermia), 35.5-36.5°C (normothermia), or 37.5-38.5°C (mild hyperthermia) throughout ischemia and re-perfusion. In normothermic animals and to a greater degree in hyperthermic animals, extracellular potassium ion activity showed delayed secondary elevation above pre-ischemia values within 40-60 min after re-perfusion. No secondary elevation of extracellular potassium ion activity was observed in hypothermic animals. There was no difference in cortical blood flow among groups with varying brain temperature, indicating that delayed deterioration of brain potassium ion homeostasis was not caused by temperature dependent alteration of cerebral blood flow. The data suggest that loss of potassium ion homeostasis during re-perfusion after focal cerebral ischemia is caused by cellular rather than vascular dysfunction and may reflect secondary inhibition of energy metabolism.

Original languageEnglish (US)
Pages (from-to)400-406
Number of pages7
JournalBrain research
Volume821
Issue number2
DOIs
StatePublished - Mar 13 1999

Keywords

  • Hydrogen clearance
  • Hyperthermia
  • Hypothermia
  • Infarction
  • K
  • Stroke

ASJC Scopus subject areas

  • Neuroscience(all)

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