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Role of endothelial glycocalyx in sliding friction at the catheter-blood vessel interface.

ABSTRACT: Catheterization is a common medical operation to diagnose and treat cardiovascular diseases. The blood vessel lumen is coated with endothelial glycocalyx layer (EGL), which is important for the permeability and diffusion through the blood vessels wall, blood hemodynamics and mechanotransduction. However EGL's role in catheter-blood vessel friction is not explored. We use a porcine aorta to mimic the blood vessel and a catheter loop was made to rub in reciprocating sliding mode against it to understand the role of catheter loop curvature, stiffness, normal load, sliding speed and EGL on the friction properties. Trypsin treatment was used to cause a degradation of the EGL. Decrease in catheter loop stiffness and EGL degradation were the strongest factors which dramatically increased the coefficient of friction (COF) and frictional energy dissipation at the aorta-catheter interface. Increasing sliding speed caused an increase but increase in normal load first caused a decrease and then an increase in the COF and frictional energy. These results provide the basic data for safety of operation and damage control during catheterization in patients with degraded EGL.

SUBMITTER: Lin C

PROVIDER: S-EPMC7366638 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Role of endothelial glycocalyx in sliding friction at the catheter-blood vessel interface.

Lin Chengxiong C Kaper Hans J HJ Li Wei W Splinter Robert R Sharma Prashant Kumar PK

Scientific reports 20200716 1

Catheterization is a common medical operation to diagnose and treat cardiovascular diseases. The blood vessel lumen is coated with endothelial glycocalyx layer (EGL), which is important for the permeability and diffusion through the blood vessels wall, blood hemodynamics and mechanotransduction. However EGL's role in catheter-blood vessel friction is not explored. We use a porcine aorta to mimic the blood vessel and a catheter loop was made to rub in reciprocating sliding mode against it to unde ...[more]

PMID: 32678286

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Project description:AimsArterial stiffness is an underlying risk factor and a hallmark of cardiovascular diseases. The endothelial cell (EC) glycocalyx is a glycan rich surface layer that plays a key role in protecting against EC dysfunction and vascular disease. However, the mechanisms by which arterial stiffness promotes EC dysfunction and vascular disease are not fully understood, and whether the mechanism involves the protective endothelial glycocalyx is yet to be determined. We hypothesized that endothelial glycocalyx protects the endothelial cells lining the vascular wall from dysfunction and disease in response to arterial stiffness.Methods and resultsCells cultured on polyacrylamide (PA) gels of substrate stiffness 10 kPa (mimicking the subendothelial stiffness of aged, unhealthy arteries) showed a significant inhibition of glycocalyx expression compared to cells cultured on softer PA gels (2.5 kPa, mimicking the subendothelial stiffness of young, healthy arteries). Specifically, gene and protein analyses revealed that a glycocalyx core protein Glypican 1 was inhibited in cells cultured on stiff PA gels. These cells had enhanced endothelial cell dysfunction as determined by enhanced cell inflammation (enhanced inflammatory gene expression, monocyte adhesion, and inhibited nitric oxide expression), proliferation, and EndMT. Removal of Glypican 1 using gene-specific silencing with siRNA or gene overexpression using a plasmid revealed that Glypican 1 is required to protect against stiffness-mediated endothelial cell dysfunction. Consistent with this, using a model of age-mediated stiffness, older mice exhibited a reduced expression of Glypican 1 and enhanced endothelial cell dysfunction compared to young mice. Glypican 1 gene deletion in knockout mice (GPC1-/-) exacerbated endothelial dysfunction in young mice, which normally had high endothelial expression, but not in old mice that normally expressed low levels. Endothelial cell dysfunction was exacerbated in young, but not aged, Glypican 1 knockout mice (GPC1-/-).ConclusionArterial stiffness promotes EC dysfunction and vascular disease at least partly through the suppression of the glycocalyx protein Glypican 1. Glypican 1 contributes to the protection against endothelial cell dysfunction and vascular disease in endothelial cells.

Project description:PurposePresent blood-contacting materials have not yet demonstrated to be effective in reducing blood coagulation without causing additional side effects clinically. We have developed an endothelial glycocalyx-inspired biomimetic surface that combines nanotopography, heparin presentation, and nitric oxide (NO)-releasing features. The resulting modified surfaces have already shown promise in reducing unfavorable blood-material interactions using platelet-rich plasma. In this study, the efficacy of modified surfaces for reducing coagulation of human whole blood was measured. In addition, the effects of leached polysaccharides and chemical modification of the modified surfaces were evaluated.MethodsLeached polysaccharides in the incubation solution were detected by a refractive index method to determine the potential influences of these modified surfaces on the blood coagulation observation. Chemical modifications by the nitrosation process on the polysaccharides in the modified surfaces were detected using attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR). Clot formation parameters were measured using thromboelastography (TEG), a clinically relevant technique to evaluate whole blood coagulation.ResultsNo polysaccharides were detected in the heparinized polyelectrolyte multilayer-coated titania nanotube array surface (TiO2NT + PEM) incubation solution; however, polysaccharides were detected from NO-releasing TiO2NT + PEM surface (TiO2NT + PEM + NO) incubation solution both after the nitrosation process and after all NO was released. The structures of thiolated chitosan and heparin were altered by t-butyl nitrite. All heparin-containing surfaces were shown to slow or inhibit clot formation.ConclusionThis study is the first to evaluate these endothelial glycocalyx-inspired surfaces using clinically relevant parameters, as well as proposing potential influences of these modified surfaces on the inhibition of clot formation.Supplementary informationThe online version contains supplementary material available at 10.1007/s44164-021-00001-w.

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Role of endothelial glycocalyx in sliding friction at the catheter-blood vessel interface.

Publications

Role of endothelial glycocalyx in sliding friction at the catheter-blood vessel interface.

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