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Glycocalyx and sepsis-induced alterations in vascular permeability.

Chelazzi C, Villa G, Mancinelli P, De Gaudio AR, Adembri C - Crit Care (2015)

Bottom Line: Sepsis-associated alterations of this structure may compromise endothelial permeability with associated interstitial fluid shift and generalized edema.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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Health Sciences, University of Florence, Section of Anesthesiology, Intensive Care and Pain Medicine, Viale Pieraccini, 6, 50139, Florence, Italy. cosimochelazzi@gmail.com.

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.

No MeSH data available.


Related in: MedlinePlus

Glycocalyx structure and the glycocalyx-endothelial barrier. ATIII, anti thrombin III; GAG, glycosaminoglycan.
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Fig1: Glycocalyx structure and the glycocalyx-endothelial barrier. ATIII, anti thrombin III; GAG, glycosaminoglycan.

Mentions: Endothelial cells line in a single layer along the inner portion of the heart, blood vessels, and lymphatic vessels. They derive from angioblasts and hemangioblasts and thus are sensitive to the mediators of angiogenesis such as vascular endothelial growth factor (VEGF) [10]. The space between two contiguous endothelial cells is called the endothelial cleft (ETC), which acts as an important site of regulation of endothelial permeability (that is, paracellular permeability) [11]. The apical side of endothelial cells is layered by the glycocalyx, which is 1 to 3 μm in depth (Figure 1). Synthesis of glycocalyx is complex, involving multiple enzymatic pathways; factors regulating its shedding include local pH and mechanical stimuli [12]. Components of glycocalyx include cell-bound proteoglycans, glycosaminoglycan (GAG) side chains, and sialoproteins [4,8,13]. Proteoglycans consist of a core protein to which GAGs are linked. Core proteins include syndecans, glypicans, and perlecans. This complex network envelops endothelial cells on their luminal side and inside the clefts, where it continues into the extracellular matrix of the basal membrane. Soluble components - that is, albumin, unbound hyaluronic acid molecules, thrombomodulin, and various serum proteins (for example, superoxide dismutase, antithrombin III, and cell adhesion molecules) - are bound to the luminal portions of glycocalyx [4].Figure 1


Glycocalyx and sepsis-induced alterations in vascular permeability.

Chelazzi C, Villa G, Mancinelli P, De Gaudio AR, Adembri C - Crit Care (2015)

Glycocalyx structure and the glycocalyx-endothelial barrier. ATIII, anti thrombin III; GAG, glycosaminoglycan.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4308932&req=5

Fig1: Glycocalyx structure and the glycocalyx-endothelial barrier. ATIII, anti thrombin III; GAG, glycosaminoglycan.
Mentions: Endothelial cells line in a single layer along the inner portion of the heart, blood vessels, and lymphatic vessels. They derive from angioblasts and hemangioblasts and thus are sensitive to the mediators of angiogenesis such as vascular endothelial growth factor (VEGF) [10]. The space between two contiguous endothelial cells is called the endothelial cleft (ETC), which acts as an important site of regulation of endothelial permeability (that is, paracellular permeability) [11]. The apical side of endothelial cells is layered by the glycocalyx, which is 1 to 3 μm in depth (Figure 1). Synthesis of glycocalyx is complex, involving multiple enzymatic pathways; factors regulating its shedding include local pH and mechanical stimuli [12]. Components of glycocalyx include cell-bound proteoglycans, glycosaminoglycan (GAG) side chains, and sialoproteins [4,8,13]. Proteoglycans consist of a core protein to which GAGs are linked. Core proteins include syndecans, glypicans, and perlecans. This complex network envelops endothelial cells on their luminal side and inside the clefts, where it continues into the extracellular matrix of the basal membrane. Soluble components - that is, albumin, unbound hyaluronic acid molecules, thrombomodulin, and various serum proteins (for example, superoxide dismutase, antithrombin III, and cell adhesion molecules) - are bound to the luminal portions of glycocalyx [4].Figure 1

Bottom Line: Sepsis-associated alterations of this structure may compromise endothelial permeability with associated interstitial fluid shift and generalized edema.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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Health Sciences, University of Florence, Section of Anesthesiology, Intensive Care and Pain Medicine, Viale Pieraccini, 6, 50139, Florence, Italy. cosimochelazzi@gmail.com.

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.

No MeSH data available.


Related in: MedlinePlus