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Editorial
. 2017 May 1;113(6):559-561.
doi: 10.1093/cvr/cvx044.

Layer upon layer: the functional consequences of disrupting the glycocalyx-endothelial barrier in vivo and in vitro

FitzRoy E Curry  1
Affiliations
Editorial

Layer upon layer: the functional consequences of disrupting the glycocalyx-endothelial barrier in vivo and in vitro

FitzRoy E Curry. Cardiovasc Res. .
No abstract available

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Figures

Figure 1
Figure 1
Contrasting views of the normal and disrupted glycocalyx. The panels show models of the glycocalyx draw from observations in intact microvessels (top) and cultured endothelial monolayers (bottom). The upper panel shows a layered structure with a dense branch-like inner layer (blue bushes) formed from heparan sulfate rich glycoproteins associated with the endothelial cell membrane (extending about 200 nm from the surface) and an outer gel-like layer, which is more porous (lightly hatched). The outer layer (up to 1 micron thick) contains adsorbed plasma proteins and other glycosaminoglycans such as hyaluronic acid. The inner layer forms the primary barrier to macromolecules (white arrow indicating limited access) and the outer layer forms the microstructure limiting access of red cells (shown) and leukocytes (not shown) to endothelial surface. The lower left panel shows the glycocalyx as described on many cultured endothelial cells (including the results in the accompanying paper1) with a less dense glycoprotein layer at the endothelial surface and no extensive outer layer of adsorbed and bound material. The right panels contrast the expected outcomes from the action of an enzyme such as heparanase on the glycocalyx of intact microvessels (top) and cultured endothelial cells (bottom). Heparanase removes heparan sulfate side chains principally from the core glycoproteins causing the bush like arrangement of these membrane-associated glycocalyx to be disrupted. This will result in changes in both the inner and outer layers of the glycocalyx but with differential effects of red cell movement (more penetration of circulating red cells into the outer layer of the glycocalyx) and transvascular vascular exchange (increased leakage of plasma proteins). These changes reflect the difference in the chemical composition and organization of both layers. These are not adequately described by the model in the lower right panel as suggested by Lukasz et al. suggesting a simple reduction in the thickness of a layer with the composition of the inner layer of the glycocalyx. Such a model will not account for changes in both red cell flows and permeability properties.
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References

    1. Lukasz A, Hillgruber C, Oberleithner H, Kusche-Vihrog K, Pavenstädt H, Rovas A, Hesse B, Goerge T, Kümpers P.. Endothelial glycocalyx breakdown is mediated by angiopoietin-2. Cardiovasc Res 2017;113:671--680. - PubMed
    1. Michel CC, Arkill KP, Curry FE.. The revised Starling principle and its relevance to peri-operative fluid management, Chapter 2. In Farag E, Kunz A (eds). Perioperative Fluid Management. Cham, Switzerland: Springer; 2016. pp. 31–74.
    1. Curry FE, Arkill KP, Michel CC.. The functions of endothelial glycocalyx and their effects on patient’s outcomes during the perioperative period. A review of current methods to evaluate structure-function relations in the glycocalyx in both basic research and clinical settings, Chapter 3. In Frag E, Kunz A (eds). Perioperative Fluid Management. Cham, Switzerland: Springer; 2016. pp. 75–116.
    1. Tarbell JM, Simon SI, Curry FE.. Mechanosensing at the vascular interface. Annu Rev Biomed Eng 2014;16:505–532. - PMC - PubMed
    1. Zeng Y, Adamson RH., Curry FE, Tarbell JM.. Sphingosine-1- phosphate protects endothelial glycocalyx by inhibiting syndecan-1 shedding. Am J Physiol Heart Circ Physiol 2014;306:H363–372. - PMC - PubMed