Ischemia and stroke.
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.
Endres
Matthias
M
Experimental Neurology, Charit, Humboldt-University of Berlin, D-10098 Berlin, Germany.
Dirnagl
Ulrich
U
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
D061945:Caspase Inhibitors; D017470:Receptors, Glutamate; D020169:Caspases