Document Detail


The endothelial glycocalyx prefers albumin for evoking shear stress-induced, nitric oxide-mediated coronary dilatation.
MedLine Citation:
PMID:  17622736     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Shear stress induces coronary dilatation via production of nitric oxide (NO). This should involve the endothelial glycocalyx (EG). A greater effect was expected of albumin versus hydroxyethyl starch (HES) perfusion, because albumin seals coronary leaks more effectively than HES in an EG-dependent way. METHODS: Isolated hearts (guinea pigs) were perfused at constant pressure with Krebs-Henseleit buffer augmented with 1/3 volume 5% human albumin or 6% HES (200/0.5 or 450/0.7). Coronary flow was also determined after EG digestion (heparinase) and with nitro-L-arginine (NO-L-Ag). RESULTS: Coronary flow (9.50 +/- 1.09, 5.10 +/- 0.49, 4.87 +/- 1.19 and 4.15 +/- 0.09 ml/min/g for 'albumin', 'HES 200', 'HES 450' and 'control', respectively, n = 5-6) did not correlate with perfusate viscosity (0.83, 1.02, 1.24 and 0.77 cP, respectively). NO-L-Ag and heparinase diminished dilatation by albumin, but not additively. Alone NO-L-Ag suppressed coronary flow during infusion of HES 450. Electron microscopy revealed a coronary EG of 300 nm, reduced to 20 nm after heparinase. Cultured endothelial cells possessed an EG of 20 nm to begin with. CONCLUSIONS: Albumin induces greater endothelial shear stress than HES, despite lower viscosity, provided the EG contains negative groups. HES 450 causes some NO-mediated dilatation via even a rudimentary EG. Cultured endothelial cells express only a rudimentary glycocalyx, limiting their usefulness as a model system.
Authors:
Matthias Jacob; Markus Rehm; Michael Loetsch; Joern O Paul; Dirk Bruegger; Ulrich Welsch; Peter Conzen; Bernhard F Becker
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-07-02
Journal Detail:
Title:  Journal of vascular research     Volume:  44     ISSN:  1423-0135     ISO Abbreviation:  J. Vasc. Res.     Publication Date:  2007  
Date Detail:
Created Date:  2007-10-24     Completed Date:  2007-11-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9206092     Medline TA:  J Vasc Res     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  435-43     Citation Subset:  IM    
Copyright Information:
Copyright 2007 S. Karger AG, Basel.
Affiliation:
Clinic of Anesthesiology, Ludwig-Maximilians-University Munich, Munich, Germany. matthias.jacob@med.uni-muenchen.de
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MeSH Terms
Descriptor/Qualifier:
Animals
Cells, Cultured
Colloids
Coronary Circulation* / drug effects
Coronary Vessels / drug effects,  metabolism*,  ultrastructure
Endothelium, Vascular / drug effects,  metabolism*,  ultrastructure
Enzyme Inhibitors / pharmacology
Glycocalyx / metabolism*,  ultrastructure
Guinea Pigs
Hemorheology
Heparin Lyase / metabolism
Hetastarch / chemistry,  metabolism*
Humans
Nitric Oxide / metabolism*
Nitric Oxide Synthase / antagonists & inhibitors,  metabolism
Nitroarginine / pharmacology
Perfusion
Plasma Substitutes / chemistry,  metabolism*
Serum Albumin / chemistry,  metabolism*
Stress, Mechanical
Time Factors
Umbilical Veins / metabolism
Vasodilation* / drug effects
Viscosity
Chemical
Reg. No./Substance:
0/Colloids; 0/Enzyme Inhibitors; 0/Plasma Substitutes; 0/Serum Albumin; 10102-43-9/Nitric Oxide; 2149-70-4/Nitroarginine; 9005-27-0/Hetastarch; EC 1.14.13.39/Nitric Oxide Synthase; EC 4.2.2.7/Heparin Lyase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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