The increase in endothelial capillary permeability represents one of the early and significant hallmarks of sepsis. An inflammatory-induced damage in endothelial glycocalyx has been identified as the mechanism involved in this increase in permeability in the condition of ischemia–reperfusion [ 1 ]. To date no data are available for glycocalyx damage in sepsis. The aim of this study was to evaluate whether sepsis-associated increase of permeability is due to glycocalyx alteration.