Heparin Impairs Glycocalyx Barrier Properties and Attenuates Shear Dependent Vasodilation in Mice
The endothelial glycocalyx is a hydrated mesh of polysaccharides and adsorbed plasma proteins that forms the true interface between the flowing blood and the endothelium. We hypothesized in the present study that competitive binding of heparin to glycocalyx-associated proteins would affect glycocaly...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2007-07, Vol.50 (1), p.261-267 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | VanTeeffelen, Jurgen W.G.E Brands, Judith Jansen, Carin Spaan, Jos A.E Vink, Hans |
| description | The endothelial glycocalyx is a hydrated mesh of polysaccharides and adsorbed plasma proteins that forms the true interface between the flowing blood and the endothelium. We hypothesized in the present study that competitive binding of heparin to glycocalyx-associated proteins would affect glycocalyx barrier properties and mechanotransduction of shear stress to the endothelium. In anesthetized mice, the clearance of 70-kDa dextrans from the circulation was increased (P |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.107.089250 |
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We hypothesized in the present study that competitive binding of heparin to glycocalyx-associated proteins would affect glycocalyx barrier properties and mechanotransduction of shear stress to the endothelium. In anesthetized mice, the clearance of 70-kDa dextrans from the circulation was increased (P<0.05 versus saline) 1 hour after heparin (1.25 U) and glycocalyx degradation with hyaluronidase (35 U; amount cleared in 30 minutes after saline11±5%; after heparin45±8%; after hyaluronidase30±3%). Clearance of 40-kDa dextrans increased (P<0.05 versus saline) to a lesser extent after both treatments (saline46±3%; heparin60±5%; hyaluronidase60±2%). The dilator response of second-order arterioles in cremaster muscle during reactive hyperemia was reduced for ≤90 minutes after heparin as reflected by a decrease (P=0.008) in t50 of diameter recovery, and this effect was associated with a diminished NO bioavailability. Infusion of hyaluronidase resulted in reductions (P<0.05) in baseline and peak reactive hyperemic diameter, whereas, despite an increase in wall shear rate at the beginning of reactive hyperemia, t50 of diameter recovery was not affected. In conclusion, our data in mice show that a heparin challenge is associated with increased vascular leakage of dextrans and impaired arteriolar vasodilation during reactive hyperemia. Our data suggest that protein–heparan sulfate interactions are important for a functional glycocalyx.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.107.089250</identifier><identifier>PMID: 17452501</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Anticoagulants - pharmacology ; Arterial hypertension. Arterial hypotension ; Arterioles - physiopathology ; Biological and medical sciences ; Biological Availability ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Dextrans - blood ; Endothelium, Vascular - physiology ; Fundamental and applied biological sciences. Psychology ; Glycocalyx - drug effects ; Glycocalyx - metabolism ; Hemodynamics. Rheology ; Heparin - pharmacology ; Hyaluronoglucosaminidase - pharmacology ; Hyperemia - chemically induced ; Hyperemia - physiopathology ; Mechanotransduction, Cellular - physiology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal - blood supply ; Nitric Oxide - metabolism ; Stress, Mechanical ; Vasodilation - drug effects ; Vertebrates: cardiovascular system</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2007-07, Vol.50 (1), p.261-267</ispartof><rights>2007 American Heart Association, Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6180-118bde8c9df46cc18a10b32234648c832ea03656acca2075ded823b7f92ea4823</citedby><cites>FETCH-LOGICAL-c6180-118bde8c9df46cc18a10b32234648c832ea03656acca2075ded823b7f92ea4823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,3674,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18870692$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17452501$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VanTeeffelen, Jurgen W.G.E</creatorcontrib><creatorcontrib>Brands, Judith</creatorcontrib><creatorcontrib>Jansen, Carin</creatorcontrib><creatorcontrib>Spaan, Jos A.E</creatorcontrib><creatorcontrib>Vink, Hans</creatorcontrib><title>Heparin Impairs Glycocalyx Barrier Properties and Attenuates Shear Dependent Vasodilation in Mice</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>The endothelial glycocalyx is a hydrated mesh of polysaccharides and adsorbed plasma proteins that forms the true interface between the flowing blood and the endothelium. We hypothesized in the present study that competitive binding of heparin to glycocalyx-associated proteins would affect glycocalyx barrier properties and mechanotransduction of shear stress to the endothelium. In anesthetized mice, the clearance of 70-kDa dextrans from the circulation was increased (P<0.05 versus saline) 1 hour after heparin (1.25 U) and glycocalyx degradation with hyaluronidase (35 U; amount cleared in 30 minutes after saline11±5%; after heparin45±8%; after hyaluronidase30±3%). Clearance of 40-kDa dextrans increased (P<0.05 versus saline) to a lesser extent after both treatments (saline46±3%; heparin60±5%; hyaluronidase60±2%). The dilator response of second-order arterioles in cremaster muscle during reactive hyperemia was reduced for ≤90 minutes after heparin as reflected by a decrease (P=0.008) in t50 of diameter recovery, and this effect was associated with a diminished NO bioavailability. Infusion of hyaluronidase resulted in reductions (P<0.05) in baseline and peak reactive hyperemic diameter, whereas, despite an increase in wall shear rate at the beginning of reactive hyperemia, t50 of diameter recovery was not affected. In conclusion, our data in mice show that a heparin challenge is associated with increased vascular leakage of dextrans and impaired arteriolar vasodilation during reactive hyperemia. Our data suggest that protein–heparan sulfate interactions are important for a functional glycocalyx.</description><subject>Animals</subject><subject>Anticoagulants - pharmacology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Arterioles - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Biological Availability</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Dextrans - blood</subject><subject>Endothelium, Vascular - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycocalyx - drug effects</subject><subject>Glycocalyx - metabolism</subject><subject>Hemodynamics. Rheology</subject><subject>Heparin - pharmacology</subject><subject>Hyaluronoglucosaminidase - pharmacology</subject><subject>Hyperemia - chemically induced</subject><subject>Hyperemia - physiopathology</subject><subject>Mechanotransduction, Cellular - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Nitric Oxide - metabolism</subject><subject>Stress, Mechanical</subject><subject>Vasodilation - drug effects</subject><subject>Vertebrates: cardiovascular system</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1Lw0AQhhdRtFb_giyCx9SdZJNsPAhVqy34hV_oKUw3E1xNk7Cbov33bmlB8ORpZ2eedxgexg5BDAASOB6_3Y8enka3j5O72-F4OACRDoTKwlhssB7EoQxknESbrCcgk0EG8LrDdp37EAKklOk224FUxh6HHsMxtWhNzSezFo11_Kpa6EZjtfjmZ2itIcvvbdOS7Qw5jnXBh11H9Rw7_318J7T8glqqC6o7_oKuKUyFnWlq7pfeGE17bKvEytH--u2z58vR0_k4uL67mpwPrwOdgBIBgJoWpHRWlDLRGhSCmEZhGMlEKq2ikFBESZyg1hiKNC6oUGE0TcvMT6Qv--xktVfbxjlLZd5aM0O7yEHkS2_5H2--n-Yrbz58sAq38-mMit_oWpQHjtYAOm-ntFhr4345pVKRZMsrTlfcV1N1ZN1nNf8im3tPVff-n0t-AM1ljQI</recordid><startdate>200707</startdate><enddate>200707</enddate><creator>VanTeeffelen, Jurgen W.G.E</creator><creator>Brands, Judith</creator><creator>Jansen, Carin</creator><creator>Spaan, Jos A.E</creator><creator>Vink, Hans</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>200707</creationdate><title>Heparin Impairs Glycocalyx Barrier Properties and Attenuates Shear Dependent Vasodilation in Mice</title><author>VanTeeffelen, Jurgen W.G.E ; Brands, Judith ; Jansen, Carin ; Spaan, Jos A.E ; Vink, Hans</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6180-118bde8c9df46cc18a10b32234648c832ea03656acca2075ded823b7f92ea4823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Anticoagulants - pharmacology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Arterioles - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Biological Availability</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Dextrans - blood</topic><topic>Endothelium, Vascular - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glycocalyx - drug effects</topic><topic>Glycocalyx - metabolism</topic><topic>Hemodynamics. Rheology</topic><topic>Heparin - pharmacology</topic><topic>Hyaluronoglucosaminidase - pharmacology</topic><topic>Hyperemia - chemically induced</topic><topic>Hyperemia - physiopathology</topic><topic>Mechanotransduction, Cellular - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Nitric Oxide - metabolism</topic><topic>Stress, Mechanical</topic><topic>Vasodilation - drug effects</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VanTeeffelen, Jurgen W.G.E</creatorcontrib><creatorcontrib>Brands, Judith</creatorcontrib><creatorcontrib>Jansen, Carin</creatorcontrib><creatorcontrib>Spaan, Jos A.E</creatorcontrib><creatorcontrib>Vink, Hans</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VanTeeffelen, Jurgen W.G.E</au><au>Brands, Judith</au><au>Jansen, Carin</au><au>Spaan, Jos A.E</au><au>Vink, Hans</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heparin Impairs Glycocalyx Barrier Properties and Attenuates Shear Dependent Vasodilation in Mice</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2007-07</date><risdate>2007</risdate><volume>50</volume><issue>1</issue><spage>261</spage><epage>267</epage><pages>261-267</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>The endothelial glycocalyx is a hydrated mesh of polysaccharides and adsorbed plasma proteins that forms the true interface between the flowing blood and the endothelium. We hypothesized in the present study that competitive binding of heparin to glycocalyx-associated proteins would affect glycocalyx barrier properties and mechanotransduction of shear stress to the endothelium. In anesthetized mice, the clearance of 70-kDa dextrans from the circulation was increased (P<0.05 versus saline) 1 hour after heparin (1.25 U) and glycocalyx degradation with hyaluronidase (35 U; amount cleared in 30 minutes after saline11±5%; after heparin45±8%; after hyaluronidase30±3%). Clearance of 40-kDa dextrans increased (P<0.05 versus saline) to a lesser extent after both treatments (saline46±3%; heparin60±5%; hyaluronidase60±2%). The dilator response of second-order arterioles in cremaster muscle during reactive hyperemia was reduced for ≤90 minutes after heparin as reflected by a decrease (P=0.008) in t50 of diameter recovery, and this effect was associated with a diminished NO bioavailability. Infusion of hyaluronidase resulted in reductions (P<0.05) in baseline and peak reactive hyperemic diameter, whereas, despite an increase in wall shear rate at the beginning of reactive hyperemia, t50 of diameter recovery was not affected. In conclusion, our data in mice show that a heparin challenge is associated with increased vascular leakage of dextrans and impaired arteriolar vasodilation during reactive hyperemia. Our data suggest that protein–heparan sulfate interactions are important for a functional glycocalyx.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>17452501</pmid><doi>10.1161/HYPERTENSIONAHA.107.089250</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 2007-07, Vol.50 (1), p.261-267 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Ovid Autoload |
| subjects | Animals Anticoagulants - pharmacology Arterial hypertension. Arterial hypotension Arterioles - physiopathology Biological and medical sciences Biological Availability Blood and lymphatic vessels Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Dextrans - blood Endothelium, Vascular - physiology Fundamental and applied biological sciences. Psychology Glycocalyx - drug effects Glycocalyx - metabolism Hemodynamics. Rheology Heparin - pharmacology Hyaluronoglucosaminidase - pharmacology Hyperemia - chemically induced Hyperemia - physiopathology Mechanotransduction, Cellular - physiology Medical sciences Mice Mice, Inbred C57BL Muscle, Skeletal - blood supply Nitric Oxide - metabolism Stress, Mechanical Vasodilation - drug effects Vertebrates: cardiovascular system |
| title | Heparin Impairs Glycocalyx Barrier Properties and Attenuates Shear Dependent Vasodilation in Mice |
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