M. Jesús Ainaga

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Reversible endotoxic shock was induced in adult rats by i.v. injection of Escherichia coli O111:B4 lipopolysaccharide (1.6 mg/100 g). The shock progression was evaluated by measuring serum glucose levels as well as activities of aspartate aminotransferase (GOT) and alkaline phosphatase in serum. A rapid increase of serum glucose levels occurs, after LPS(More)
Oxygen-derived radicals have been suggested to produce tissue injury during endotoxic shock by initiating lipid peroxidation. In order to investigate the induction of lipid peroxidation by Escherichia coli 0111:B4 lipopolysaccharide (LPS) on hepatocytes, malondialdehyde (MDA) and superoxide dismutase (SOD) activity have been evaluated in vivo and in vitro(More)
In this study, the fluorescent Ca2+ probe fura-2 and the fluorescent pH indicator BCECF have been used to monitor cytosolic free Ca2+ and intracellular pH (pHi), respectively, in isolated and cultured hepatocytes treated with Escherichia coli O111:B4 endotoxin. Uptake of 45Ca2+ was also measured to study the effect of endotoxin on the extracellular calcium(More)
Cytotoxic lesions, induced by Gram-negative lipopolysaccharides (LPS), occur mainly in liver where the microsomal compartment of hepatocytes is involved in the detoxification mechanisms as well as in the biosynthesis of different active metabolites. The alterations induced by LPS from E. coli 0111: 134 on cytochrome b5 and its correlation with cytochrome(More)
Reversible endotoxic shock was induced in adult rats by intravenous injection of E. coli 0111:B4 lipopolysaccharide (LPS) and the progression of metabolic and morphological alterations was evaluated. Serum samples and biopsies from adrenal gland, liver and lung were studied at different times after LPS injection. Histological changes in these tissues were(More)
During endotoxic shock, the liver exerts a lipopolysaccharide (LPS) clearance function with the participation of both parenchymal and sinusoidal cells. Liver damage could be caused by LPS direct action, hypoxia and/or inflammatory mediators released by Kupffer cells. The aim of this study is to establish an experimental model that could allow us to(More)
In order to clarify the endotoxin effect on the hepatic removal of insulin, the influence of lipopolysaccharide (LPS) from E. coli 0111:B4 on the insulin binding and endocytosis in cultured hepatocytes from adult male rats has been investigated. LPS decreases both processes in a time and temperature-dependent manner, showing a major effect at short time and(More)
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