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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...
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| Autori principali: | , , , , |
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| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
1994
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC42929/ https://ncbi.nlm.nih.gov/pubmed/7506416 |
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