title: The endothelial glycocalyx prefers albumin for evoking shear stress-induced, nitric oxide-mediated coronary dilatation.
abstract: 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.affiliation: Clinic of Anesthesiology, Ludwig-Maximilians-University Munich, Munich, Germany. matthias.jacob@med.uni-muenchen.de
authors.forename: Matthias
authors.initials: M
authors.lastname: Jacob
authors.forename: Markus
authors.initials: M
authors.lastname: Rehm
authors.forename: Michael
authors.initials: M
authors.lastname: Loetsch
authors.forename: Joern O
authors.initials: JO
authors.lastname: Paul
authors.forename: Dirk
authors.initials: D
authors.lastname: Bruegger
authors.forename: Ulrich
authors.initials: U
authors.lastname: Welsch
authors.forename: Peter
authors.initials: P
authors.lastname: Conzen
authors.forename: Bernhard F
authors.initials: BF
authors.lastname: Becker
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D003102:Colloids; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D004791:Enzyme Inhibitors / Q000494:pharmacology; D019276:Glycocalyx / Q000378:metabolism* / Q000648:ultrastructure; D006168:Guinea Pigs; D018056:Hemorheology; D019763:Heparin Lyase / Q000378:metabolism; D006801:Humans; D006895:Hydroxyethyl Starch Derivatives / Q000737:chemistry / Q000378:metabolism*; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D019335:Nitroarginine / Q000494:pharmacology; D010477:Perfusion; D010952:Plasma Substitutes / Q000737:chemistry / Q000378:metabolism*; D012709:Serum Albumin / Q000737:chemistry / Q000378:metabolism*; D013314:Stress, Mechanical; D013997:Time Factors; D014471:Umbilical Veins / Q000378:metabolism; D014664:Vasodilation / Q000187:drug effects; D014783:Viscosity
chemical_list: D003102:Colloids; D004791:Enzyme Inhibitors; D006895:Hydroxyethyl Starch Derivatives; D010952:Plasma Substitutes; D012709:Serum Albumin; D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019763:Heparin Lyase