Abstract
Endothelial cells line the inner portion of the heart, blood vessels, and lymphatic vessels; a basal membrane of extracellular matrix lines the extraluminal side of endothelial cells. The apical side of endothelial cells is the site for the glycocalyx, which is a complex network of macromolecules, including cell-bound proteoglycans and sialoproteins. Sepsis-associated alterations of this structure may compromise endothelial permeability with associated interstitial fluid shift and generalized edema. Indeed, in sepsis, the glycocalyx acts as a target for inflammatory mediators and leukocytes, and its ubiquitous nature explains the damage of tissues that occurs distant from the original site of infection. Inflammatory-mediated injury to glycocalyx can be responsible for a number of specific clinical effects of sepsis, including acute kidney injury, respiratory failure, and hepatic dysfunction. Moreover, some markers of glycocalyx degradation, such as circulating levels of syndecan or selectins, may be used as markers of endothelial dysfunction and sepsis severity. Although a great deal of experimental evidence shows that alteration of glycocalyx is widely involved in endothelial damage caused by sepsis, therapeutic strategies aiming at preserving its integrity did not significantly improve the outcome of these patients.
Highlights
Sepsis is the clinical syndrome of a systemic response to microbial infections
Exposure to pro-inflammatory mediators such as interleukin 1 (IL-1), IL-2, IL-6, Tumor necrosis factor-alpha (TNF-α), and other molecules released during acute inflammation such as bradykinin, thrombin, vascular endothelial growth factor (VEGF), and histamine results in endothelial activation and massive increase in glycocalyx expression of endothelial leukocyte adhesion molecule 1, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1)
Interaction of syndecans with TNF-α leads to a structural rearrangement of endothelial cells and loosening of intercellular junctions; this greatly increases paracellular permeability, further allowing extravasations of fluids, albumin, and solutes [2]
Summary
Sepsis is the clinical syndrome of a systemic response to microbial infections. During septic shock, mortality can peak at 56% [1,2]. Sepsis is associated with altered micro-hemodynamics and heterogeneous local perfusion, micro-thrombosis and endothelial dysfunction, alteration of permeability, and interstitial fluid shift [3,4,5,6]. In clinical conditions of increased capillary porosity, like sepsis, albumin and other proteins may reach the extravascular space and, πis rises and the flow of fluid increases.
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