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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.

The Endothelial Glycocalyx Prefers Albumin for Evoking Shear Stress-Induced, Nitric Oxide-Mediated Coronary Dilatation