ArticleFrontiers in physiology2018
Implications Enzymatic Degradation of the Endothelial Glycocalyx on the Microvascular Hemodynamics and the Arteriolar Red Cell Free Layer of the Rat Cremaster Muscle.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Review on Blood Flow Dynamics in Lab-on-a-Chip Systems: An Engineering Perspective.Chem & bio engineering · 2024Review
- Unraveling neurovascular mysteries: the role of endothelial glycocalyx dysfunction in Alzheimer's disease pathogenesis.Frontiers in physiology · 2024Review
- Endothelial glycocalyx in retina, hyperglycemia, and diabetic retinopathy.American journal of physiology. Cell physiology · 2023Review
- Control of systemic inflammation through early nitric oxide supplementation with nitric oxide releasing nanoparticles.Free radical biology & medicine · 2020Article
- Role of endothelial glycocalyx in sliding friction at the catheter-blood vessel interface.Scientific reports · 2020Article
- Label-free assessment of hemodynamics in individual cortical brain vessels using third harmonic generation microscopy.Biomedical optics express · 2020Article
- Cellular microdomains for nitric oxide signaling in endothelium and red blood cells.Nitric oxide : biology and chemistry · 2020Review
- Resuscitation After Hemorrhagic Shock in the Microcirculation: Targeting Optimal Oxygen Delivery in the Design of Artificial Blood Substitutes.Frontiers in medicine · 2020Review
- Biophysical and biomolecular interactions of malaria-infected erythrocytes in engineered human capillaries.Science advances · 2020Article
- Postoperative microcirculatory perfusion and endothelial glycocalyx shedding following cardiac surgery with cardiopulmonary bypass.Anaesthesia · 2019Observational
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
The endothelial glycocalyx is a complex network of glycoproteins, proteoglycans, and glycosaminoglycans; it lines the vascular endothelial cells facing the lumen of blood vessels forming the endothelial glycocalyx layer (EGL). This study aims to investigate the microvascular hemodynamics implications of the EGL by quantifying changes in blood flow hydrodynamics post-enzymatic degradation of the glycocalyx layer. High-speed intravital microscopy videos of small arteries (around 35 μm) of the rat cremaster muscle were recorded at various time points after enzymatic degradation of the EGL. The thickness of the cell free layer (CFL), blood flow velocity profiles, and volumetric flow rates were quantified. Hydrodynamic effects of the presence of the EGL were observed in the differences between the thickness of CFL in microvessels with an intact EGL and glass tubes of similar diameters. Maximal changes in the thickness of CFL were observed 40 min post-enzymatic degradation of the EGL. Analysis of the frequency distribution of the thickness of CFL allows for estimation of the thickness of the endothelial surface layer (ESL), the plasma layer, and the glycocalyx. Peak flow, maximum velocity, and mean velocity were found to statistically increase by 24, 27, and 25%, respectively, after enzymatic degradation of the glycocalyx. The change in peak-to-peak maximum velocity and mean velocity were found to statistically increase by 39 and 32%, respectively, after 40 min post-enzymatic degradation of the EGL. The bluntness of blood flow velocity profiles was found to be reduced post-degradation of the EGL, as the exclusion volume occupied by the EGL increased the effective volume impermeable to RBCs in microvessels. This study presents the effects of the EGL on microvascular hemodynamics. Enzymatic degradation of the EGL resulted in a decrease in the thickness of CFL, an increase in blood velocity, blood flow, and decrease of the bluntness of the blood flow velocity profile in small arterioles. In summary, the EGL functions as a molecular sieve to solute transport and as a lubrication layer to protect the endothelium from red blood cell (RBC) motion near the vessel wall, determining wall shear stress.
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