Ischemia and stroke

Adv Exp Med Biol. 2002:513:455-73. doi: 10.1007/978-1-4615-0123-7_17.

Abstract

Cell death following cerebral ischemia is mediated by a complex pathophysiologic interaction of different mechanisms. In this Chapter we will outline the basic principles as well as introduce in vitro and in vivo models of cerebral ischemia. Mechanistically, excitotoxicity, peri-infarct depolarization, inflammation and apoptosis seem to be the most relevant mediators of damage and are promising targets for neuroprotective strategies.

Publication types

  • Review

MeSH terms

  • Acidosis
  • Animals
  • Apoptosis
  • Brain / metabolism*
  • Brain / pathology*
  • Brain Ischemia* / metabolism
  • Brain Ischemia* / pathology
  • Brain Ischemia* / physiopathology
  • Caspase Inhibitors
  • Caspases / metabolism
  • Disease Models, Animal
  • Humans
  • Inflammation / metabolism
  • Necrosis
  • Receptors, Glutamate / metabolism
  • Stroke* / metabolism
  • Stroke* / pathology
  • Stroke* / physiopathology
  • Temperature

Substances

  • Caspase Inhibitors
  • Receptors, Glutamate
  • Caspases