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Attenuation of the induction of nitric oxide synthase by endogenous glucocorticoids accounts for endotoxin tolerance in vivo.

An enhanced formation of nitric oxide (NO) due to induction of a calcium-independent (inducible) NO synthase (iNOS) contributes importantly to the cardiovascular failure caused by bacterial endotoxin. Repeated challenges with small doses of endotoxin result in tolerance to both peripheral vascular f...

Täydet tiedot

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Bibliografiset tiedot
Päätekijät: Szabó, C, Thiemermann, C, Wu, C C, Perretti, M, Vane, J R
Aineistotyyppi: Artigo
Kieli:Inglês
Julkaistu: 1994
Aiheet:
Linkit:https://ncbi.nlm.nih.gov/pmc/articles/PMC42929/
https://ncbi.nlm.nih.gov/pubmed/7506416
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