title: [Biochemistry of cerebral ischemia].
abstract: The fall in cerebral blood flow beneath certain critical values causes a rapid depletion in energy together with changes in cerebral function, and sets off a complex chain of biochemical changes that cause cell death. These biochemical changes depend fundamentally on two mechanisms: the development of acidosis and the entry of ionic calcium into the cell. The rise in intracellular calcium activates the phospholipases, proteases, and nitric oxide synthetases, and initiates the immediate early genes expression. Knowledge of these mechanisms and the possibility of modifying the chain of events leading to cell death constitute the basis of neuroprotection.
authors.affiliation: Servicio de Neurología, Hospital Xeral de Galicia, Universidad de Santiago de Compostela. mecasti@usc.es
authors.forename: J
authors.initials: J
authors.lastname: Castillo
mesh_terms: D000140:Acidosis, Lactic / Q000209:etiology; D001921:Brain / Q000098:blood supply / Q000378:metabolism*; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000502:physiology*; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D018091:Receptors, AMPA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
chemical_list: D015220:Calcium Channels; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D019344:Lactic Acid