A compromising endothelial cell (EC) monolayer affects vascular permeability and leads to fluid extravasation. Tight junctions and more particularly Zonula occludens 1 (ZO-1) play a major role in maintaining vascular barrier integrity and are regulated by cytoskeletal proteins. During sepsis, endothelial barrier disruption occurs in most organs and contributes to organ dysfunction. We and others have demonstrated that the α1 isoform of AMP-activated protein kinase (α1AMPK) controls cytoskeleton organisation in various cell types including endothelial cells. Therefore, we hypothesised that α1AMPK preserves tight junction organisation and vascular permeability during sepsis in the coronary microcirculation.