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Oxygen tension-independent protection against hypoxic cell killing in rat liver by low sodium

The role of Na(+) in hypoxic injury was evaluated by a time-course analysis of damage in isolated livers perfused with N(2)-saturated buffer containing standard (143 mM) or low (25 mM) Na(+) levels. Trypan blue uptake was used to detect non-viable cells. Under hypoxia with standard-Na(+), trypan blu...

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Detalles Bibliográficos
Autores principales: Ferrigno, Andrea, Pasqua, Laura G. Di, Berardo, Clarissa, Siciliano, Veronica, Richelmi, Plinio, Vairetti, Mariapia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PAGEPress Publications, Pavia, Italy 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452633/
https://www.ncbi.nlm.nih.gov/pubmed/28735525
http://dx.doi.org/10.4081/ejh.2017.2798
Descripción
Sumario:The role of Na(+) in hypoxic injury was evaluated by a time-course analysis of damage in isolated livers perfused with N(2)-saturated buffer containing standard (143 mM) or low (25 mM) Na(+) levels. Trypan blue uptake was used to detect non-viable cells. Under hypoxia with standard-Na(+), trypan blue uptake began at the border between pericentral areas and periportal regions and increased in the latter zone; using a low-Na(+) buffer, no trypan blue zonation occurred but a homogenous distribution of dye was found associated with sinusoidal endothelial cell (SEC) staining. A decrease in hyaluronic acid (HA) uptake, index of SEC damage, was observed using a low-Na(+) buffer. A time dependent injury was confirmed by an increase in LDH and TBARS levels with standard-Na(+) buffer. Using low-Na(+) buffer, SEC susceptibility appears elevated under hypoxia and hepatocytes was protected, in an oxygen independent manner.