Publication:
Implications enzymatic degradation of the endothelial glycocalyx on the microvascular hemodynamics and the arteriolar red cell free layer of the rat cremaster muscle

dc.contributor.coauthorJani, Vivek P.
dc.contributor.coauthorJohnson, Paul C.
dc.contributor.coauthorCabrales, Pedro
dc.contributor.departmentSchool of Medicine
dc.contributor.kuauthorYalçın, Özlem
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2024-11-09T12:15:06Z
dc.date.issued2018
dc.description.abstractThe 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 mu m) 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 40min 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 40min 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.
dc.description.fulltextYES
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipNIH grants from the Heart Lung and Blood Institute
dc.description.versionPublisher version
dc.description.volume9
dc.identifier.doi10.3389/fphys.2018.00168
dc.identifier.eissn1664-042X
dc.identifier.embargoNO
dc.identifier.filenameinventorynoIR01416
dc.identifier.quartileQ2
dc.identifier.scopus2-s2.0-85043999519
dc.identifier.urihttps://doi.org/10.3389/fphys.2018.00168
dc.identifier.wos427619800001
dc.keywordsCell free layer
dc.keywordsEndothelial glycocalyx
dc.keywordsEndothelial surface layer
dc.keywordsPlasma layer
dc.keywordsEnzymatic degradation
dc.keywordsBlood flow
dc.keywordsShear stress
dc.keywordsMicrocirculation
dc.language.isoeng
dc.publisherFrontiers
dc.relation.grantnoP01-HL11090
dc.relation.grantnoR01HL126945
dc.relation.grantnoR01HL138116
dc.relation.ispartofFrontiers in Physiology
dc.relation.urihttp://cdm21054.contentdm.oclc.org/cdm/ref/collection/IR/id/8008
dc.subjectPhysiology
dc.titleImplications enzymatic degradation of the endothelial glycocalyx on the microvascular hemodynamics and the arteriolar red cell free layer of the rat cremaster muscle
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorYalçın, Özlem
local.publication.orgunit1SCHOOL OF MEDICINE
local.publication.orgunit2School of Medicine
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relation.isOrgUnitOfPublication.latestForDiscoveryd02929e1-2a70-44f0-ae17-7819f587bedd
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