Postischemic hyperthermia induced caspase-3 activation in the newborn rat brain after hypoxia-ischemia and exacerbated the brain damage

Biol Neonate. 2003;84(2):164-71. doi: 10.1159/000071952.

Abstract

The effects of postischemic hyperthermia were investigated in the newborn rat brain after hypoxia-ischemia (HI). Seven-day-old rats were subjected to left carotid artery ligation followed by 8% oxygen for 30 min, and divided into a hyperthermia group (rectal temperature at 39 degrees C for 6 h) and a normothermia group. Hyperthermia resulted in an approximately 5-fold increase in activated caspase-3 24 h after HI when compared with the normothermia group, and gross loss of brain tissue was observed only in the hyperthermia group at 7 and 30 days after HI. Our results show that postischemic hyperthermia exacerbates HI injury in immature brains, and that the mechanism is strongly associated with activation of an apoptotic pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn*
  • Apoptosis
  • Body Temperature
  • Brain Diseases / etiology*
  • Brain Diseases / pathology
  • Caspase 3
  • Caspases / metabolism*
  • Enzyme Activation
  • Female
  • Hyperthermia, Induced / adverse effects*
  • Hypoxia-Ischemia, Brain / complications*
  • Male
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Casp3 protein, rat
  • Caspase 3
  • Caspases