02 July 2007
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.