[Pathophysiology of cerebral ischemia].
After cerebral ischemia, brain cells are injured by a number of different mechanisms. While the blood flow disturbance and consecutive energy depletion, is the initial event, excitotoxicity, peri-infarct-depolarisations, inflammation and apoptosis are most important subsequently. In this review, current knowledge on these events is summarized and it will be outlined how future treatment strategies can be derived from this knowledge.
Neurologische Klinik, Charité, Humboldt-Universität Berlin.
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Villringer
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Dirnagl
D017209:Apoptosis / Q000502:physiology; D001921:Brain / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology*; D002544:Cerebral Infarction / Q000503:physiopathology; D018846:Excitatory Amino Acids / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D009474:Neurons / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology
D018846:Excitatory Amino Acids; D018836:Inflammation Mediators
Pathophysiologie der zerebralen Ischämie.