title: Role of nitric oxide after brain ischaemia.
abstract: Ischaemic stroke is the second or third leading cause of death in developed countries. In the last two decades substantial research and efforts have been made to understand the biochemical mechanisms involved in brain damage and to develop new treatments. The evidence suggests that nitric oxide (NO) can exert both protective and deleterious effects depending on factors such as the NOS isoform and the cell type by which NO is produced or the temporal stage after the onset of the ischaemic brain injury. Immediately after brain ischaemia, NO release from eNOS is protective mainly by promoting vasodilation; however, after ischaemia develops, NO produced by overactivation of nNOS and, later, NO release by de novo expression of iNOS contribute to the brain damage. This review article summarizes experimental and clinical data supporting the dual role of NO in brain ischaemia and the mechanisms by which NO is regulated after brain ischaemia. We also review NO-based therapeutic strategies for stroke treatment, not only those directly linked with the NO pathway such as NO donors and NOS inhibitors but also those partially related like statins, aspirin or lubeluzole.
authors.affiliation: Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid, 28040 Madrid, Spain.
authors.forename: M A
authors.initials: MA
authors.lastname: Moro
authors.forename: A
authors.initials: A
authors.lastname: Cárdenas
authors.forename: O
authors.initials: O
authors.lastname: Hurtado
authors.forename: J C
authors.initials: JC
authors.lastname: Leza
authors.forename: I
authors.initials: I
authors.lastname: Lizasoain
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000502:physiology; D052247:Nitric Oxide Synthase Type II
chemical_list: D009569:Nitric Oxide; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II