Amelioration of Ischemic brain damage by peritoneal dialysis

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dc.contributor.author Del Carmen Godino, María
dc.contributor.author Romera, Víctor G.
dc.contributor.author Sánchez-Tomero, José Antonio
dc.contributor.author Pacheco, Jesus
dc.contributor.author Canals, Santiago
dc.contributor.author Lerma, Juan
dc.contributor.author Vivancos, José Carlos
dc.contributor.author Moro, María Ángeles
dc.contributor.author Torres, Magdalena
dc.contributor.author Lizasoaín, Ignacio
dc.contributor.author Sánchez-Prieto, José
dc.contributor.other UAM. Departamento de Medicina es_ES
dc.date.accessioned 2015-02-17T11:17:08Z
dc.date.available 2015-02-17T11:17:08Z
dc.date.issued 2013-10-01
dc.identifier.citation The Journal of Clinical Investigation 123.10 (2013): 4359-4363 en_US
dc.identifier.issn 0021-9738 (print) en_US
dc.identifier.issn 1558-8238 (online) en_US
dc.identifier.uri http://hdl.handle.net/10486/663877
dc.description.abstract Ischemic stroke is a devastating condition, for which there is still no effective therapy. Acute ischemic stroke is associated with high concentrations of glutamate in the blood and interstitial brain fluid. The inability of the tissue to retain glutamate within the cells of the brain ultimately provokes neuronal death. Increased concentrations of interstitial glutamate exert further excitotoxic effects on healthy tissue surrounding the infarct zone. We developed a strategy based on peritoneal dialysis to reduce blood glutamate levels, thereby accelerating brain-to-blood glutamate clearance. In a rat model of stroke, this simple procedure reduced the transient increase in glutamate, consequently decreasing the size of the infarct area. Functional magnetic resonance imaging demonstrated that the rescued brain tissue remained functional. Moreover, in patients with kidney failure, peritoneal dialysis significantly decreased glutamate concentrations. Our results suggest that peritoneal dialysis may represent a simple and effective intervention for human stroke patients en_US
dc.description.sponsorship This work was supported by grants from the Spanish MINECO to J. Sánchez-Prieto (BFU2010/16947), I. Lizasoain (SAF2011- 23354), and M.A. Moro (SAF2009-08145, SAF2012-33216, and CSD2010-00045); from Fondo Europeo de Desarrollo Regional (FEDER) “Instituto de Salud Carlos III” (RD06/0026, RD12/0014) to I. Lizasoain, M. Torres, J. Vivancos, and J. Sánchez-Prieto; from the “Comunidad de Madrid” (CAM-I2M2 2011-BMD-2349) to I. Lizasoain, M. Torres, J. Vivancos, and J. Sánchez-Prieto; and from NEUROSTEMCM to M.A. Moro (S2010/BMD-2336). Research in the laboratory of S. Canals and J. Lerma is supported by grants from the Spanish MINECO (BFU2009-09938, BFU2011-24084, and CSD2007-00023) en_US
dc.format.extent 5 pag. es_ES
dc.format.mimetype application/pdf en
dc.language.iso eng en
dc.publisher American Society for Clinical Investigation en_US
dc.relation.ispartof Journal of Clinical Investigation en_US
dc.subject.other brain hemorrhage en_US
dc.subject.other brain ischemia en_US
dc.subject.other chronic kidney disease en_US
dc.subject.other peritoneal dialysis en_US
dc.subject.other endothelium cell en_US
dc.title Amelioration of Ischemic brain damage by peritoneal dialysis en_US
dc.type article en
dc.subject.eciencia Medicina es_ES
dc.identifier.doi 10.1172/JCI67284 es_ES
dc.identifier.publicationfirstpage 4359 es_ES
dc.identifier.publicationissue 10 es_ES
dc.identifier.publicationlastpage 4363 es_ES
dc.identifier.publicationvolume 123 es_ES
dc.relation.projectID Comunidad de Madrid. S2010/BMD-2336/NEUROSTEM es_ES
dc.relation.projectID Comunidad de Madrid. S2010/BMD-2349/I2M2 es_ES
dc.type.version info:eu-repo/semantics/publishedVersion en
dc.rights.accessRights openAccess en


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