作者
Diego Castanares-Zapatero, Claire Bouleti, Caroline Sommereyns, Bernhard Gerber, Christelle Lecut, Thomas Mathivet, Michael Horckmans, Didier Communi, Marc Foretz, Jean-Louis Vanoverschelde, Stéphane Germain, Luc Bertrand, Pierre-François Laterre, Cecile Oury, Benoit Viollet, Sandrine Horman, Christophe Beauloye
发表日期
2013/12/1
期刊
Critical care medicine
卷号
41
期号
12
页码范围
e411-e422
出版商
LWW
简介
Objective:
As adenosine monophosphate (AMP)-activated protein kinase both controls cytoskeleton organization in endothelial cells and exerts anti-inflammatory effects, we here postulated that it could influence vascular permeability and inflammation, thereby counteracting cardiac wall edema during sepsis.
Design:
Controlled animal study.
Settings:
University research laboratory.
Subjects:
C57BL/6J, α 1 AMPK–/–, and α 1 AMPK+/+ mice.
Intervention:
Sepsis was triggered in vivo using a sublethal injection of lipopolysaccharide (O55B5, 10 mg/kg), inducing systolic left ventricular dysfunction. Left ventricular function, edema, vascular permeability, and inflammation were assessed in vivo in both wild-type mice (α 1 AMPK+/+) and α 1 AMP-activated protein kinase–deficient mice (α 1 AMPK–/–). The 5-aminoimidazole-4-carboxamide riboside served to study the impact of AMP-activated protein kinase activation on …
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