The endothelial glycocalyx prefers albumin for evoking shear stress-induced, nitric oxide-mediated coronary dilatation

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. Copyright (c) 2007 S. Karger AG, Basel.