2006/02/01 by Max Nieuwdorp, Timon W. van Haeften, Mirella Gouverneur +9 · 1 voice · 632 citations
Chemistry · Medicine · #Acute Ischemic Stroke Management #Biochemistry #Biology #Chemistry #Endocrinology #Endothelial dysfunction #Endothelium #Glycocalyx #Immunology #In vivo #Internal medicine #Mannitol #Medicine #Trauma, Hemostasis, Coagulopathy, Resuscitation #Traumatic Brain Injury and Neurovascular Disturbances
paper · pdf · doi:10.2337/diabetes.55.02.06.db05-1103
published in Diabetes 55(2), 480-486 (American Diabetes Association)
openalex publication_date 2006/02/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/05
Hyperglycemia is associated with increased susceptibility to atherothrombotic stimuli. The glycocalyx, a layer of proteoglycans covering the endothelium, is involved in the protective capacity of the vessel wall. We therefore evaluated whether hyperglycemia affects the glycocalyx, thereby increasing vascular vulnerability. The systemic glycocalyx volume was estimated by comparing the distribution volume of a glycocalyx permeable tracer (dextran 40) with that of a glycocalyx impermeable tracer (labeled erythrocytes) in 10 healthy male subjects. Measurements were performed in random order on five occasions: two control measurements, two measurements during normoinsulinemic hyperglycemia with or without N-acetylcysteine (NAC) infusion, and one during mannitol infusion. Glycocalyx measurements were reproducible (1.7 +/- 0.2 vs. 1.7 +/- 0.3 l). Hyperglycemia reduced glycocalyx volume (to 0.8 +/- 0.2 l; P < 0.05), and NAC was able to prevent the reduction (1.4 +/- 0.2 l). Mannitol infusion had no effect on glycocalyx volume (1.6 +/- 0.1 l). Hyperglycemia resulted in endothelial dysfunction, increased plasma hyaluronan levels (from 70 +/- 6 to 112 +/- 16 ng/ml; P < 0.05) and coagulation activation (prothrombin activation fragment 1 + 2: from 0.4 +/- 0.1 to 1.1 +/- 0.2 nmol/l; d-dimer: from 0.27 +/- 0.1 to 0.55 +/- 0.2 g/l; P < 0.05). Taken together, these data indicate a potential role for glycocalyx perturbation in mediating vascular dysfunction during hyperglycemia.