title: Ischemia and stroke.
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.
authors.affiliation: Experimental Neurology, Charit, Humboldt-University of Berlin, D-10098 Berlin, Germany.
authors.forename: Matthias
authors.initials: M
authors.lastname: Endres
authors.forename: Ulrich
authors.initials: U
authors.lastname: Dirnagl
mesh_terms: D000138:Acidosis; D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000378:metabolism* / Q000473:pathology*; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D061945:Caspase Inhibitors; D020169:Caspases / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D009336:Necrosis; D017470:Receptors, Glutamate / Q000378:metabolism; D020521:Stroke / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013696:Temperature
chemical_list: D061945:Caspase Inhibitors; D017470:Receptors, Glutamate; D020169:Caspases