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Benoit Vallet

Researcher at university of lille

Publications -  192
Citations -  9098

Benoit Vallet is an academic researcher from university of lille. The author has contributed to research in topics: Septic shock & Intensive care. The author has an hindex of 48, co-authored 192 publications receiving 8281 citations. Previous affiliations of Benoit Vallet include University of Alabama at Birmingham.

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Journal Article

Effects of nitric oxide synthase inhibition on regional hemodynamics and oxygen transport in endotoxic dogs.

TL;DR: The data suggest that in acute endotoxicosis, L‐Name may significantly improve blood pressure but may markedly encroach on O2 transport reserves to the gut.
Journal ArticleDOI

Pretreatment with peroxysome proliferator-activated receptor α agonist fenofibrate protects endothelium in rabbit Escherichia coli endotoxin-induced shock

TL;DR: These data indicate for the first time that fenofibrate, an activator of PPAR-α, inhibits monocyte tissue factor expression and protects against endothelial dysfunction and histological injury in endotoxin-induced shock.
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French multicentre survey on the use of inotropes after cardiac surgery.

Olivier Bastien, +1 more
- 23 Feb 2005 - 
TL;DR: Results from a French multicentre survey on the use of inotropes after cardiac surgery are presented and the importance of developing monitoring strategies to help in decision making regarding therapy with inotrope in this context is highlighted.
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EuSOS: European surgical outcomes study.

TL;DR: From Queen Mary’s University of London (RMP), St George's Hospital (AR), London, UK, Hospital de Santo António dos Capuchos, Lisbon, Portugal (RM), University of Insubria, Varese, Italy (PP), Charité Universitätsmedizin, Berlin, Germany (CS), Centre Hospitalier Universitaire de Lille, Lilles, France (BV).
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Activation of peroxisome proliferator-activated receptor-α by fenofibrate prevents myocardial dysfunction during endotoxemia in rats

TL;DR: Fenofibrate, an activator of peroxisome proliferator-activated receptor-α, may prevent endotoxemia-induced cardiac dysfunction and reduction in myofilament Ca2+ sensitivity and the data suggest a mediating role for early peak plasma tumor necrosis factor-α but not for myocardial NO production or oxidative stress.