Hepatic encephalopathy-associated cerebral vasculopathy in acute-on-chronic liver failure: Alterations on endothelial factor release and influence on cerebrovascular function
Entidad
UAM. Departamento de Cirugía; UAM. Departamento de Farmacología; UAM. Departamento de Fisiología; Instituto de Investigación Sanitaria Hospital Universitario de La Paz (IdiPAZ)Editor
Frontiers MediaFecha de edición
2020-11-20Cita
10.3389/fphys.2020.593371
Frontiers in Physiology 11.Nov (2020): 593371
ISSN
1664-042XDOI
10.3389/fphys.2020.593371Financiado por
This research was funded by the Ministerio de Economía y Competitividad (SAF2016-80305-P), CiberCV (Grant number: CB16/11/00286), the European Regional Development Grant (FEDER) (Comunidad de Madrid, grant number B2017/BMD- 3676), and R C D projects for young researchers, Universidad Autónoma de Madrid-Comunidad de Madrid (SI1-PJI-2019- 00321). RR-D received a fellowship from Juan de la Cierva Program (IJCI-2017-31399).Proyecto
Gobierno de España. SAF2016-80305-P; Gobierno de España. CB16/11/00286; Comunidad de Madrid. B2017/BMD-3676/AORTASANAVersión del editor
http://doi.org/10.3389/fphys.2020.593371Materias
acute-on-chronic liver failure; bradykinin; cerebral vasculature; hepatic encephalopathy; nitric oxide; prostaglandin I 2; MedicinaDerechos
© 2020 Caracuel, Sastre, Callejo, Rodrigues-Díez, García-Redondo, Prieto, Nieto, Salaices, Aller, Arias and Blanco-Rivero.Resumen
The acute-on-chronic liver failure (ACLF) is a syndrome characterized by liver decompensation, hepatic encephalopathy (HE) and high mortality. We aimed to determine the mechanisms implicated in the development of HE-associated cerebral vasculopathy in a microsurgical liver cholestasis (MHC) model of ACLF. Microsurgical liver cholestasis was induced by ligating and extracting the common bile duct and four bile ducts. Sham-operated and MHC rats were maintained for eight postoperative weeks Bradykinin-induced vasodilation was greater in middle cerebral arteries from MHC rats. Both Nω-Nitro-L-arginine methyl ester and indomethacin diminished bradykinin-induced vasodilation largely in arteries from MHC rats. Nitrite and prostaglandin (PG) F releases were increased, whereas thromboxane (TX) B was not modified in arteries from MHC. Expressions of endothelial nitric oxide synthase (eNOS), inducible NOS, and cyclooxygenase (COX) 2 were augmented, and neuronal NOS (nNOS), COX-1, PGI synthase, and TXA S were unmodified. Phosphorylation was augmented for eNOS and unmodified for nNOS. Altogether, these endothelial alterations might collaborate to increase brain blood flow in HE. 1α 2 2 2
Lista de ficheros
Google Scholar:Caracuel, Laura
-
Sastre, Esther
-
Callejo, María
-
Rodrigues Díez, Raquel
-
García Redondo, Ana Belén
-
Prieto Nieto, María Isabel
-
Nieto, Carlos
-
Salaices Sánchez, Mercedes
-
Aller, Ma Ángeles
-
Arias, Jaime
-
Blanco Rivero, Javier
Lista de colecciones del ítem
Registros relacionados
Mostrando ítems relacionados por título, autor, creador y materia.