Constituents of vascular endothelial surface layer (glycocalyx), e.g. an anchor protein syndecan-1 (SDC-1), can be detected in plasma in many inflammatory conditions. In inflammation, vascular adhesion protein-1 (VAP-1) is rapidly translocated to the apical side of the endothelial cells and may be released to plasma in a soluble form. We hypothesized that glycocalyx injury coincides with VAP-1 activation on endothelial cells. To test the hypothesis, we measured SDC-1 and VAP-1 levels in 20 patients with septic shock.
A prospective observational study was conducted in two multidisciplinary critical care units in two tertiary academic teaching hospitals with 20 mechanically ventilated adult patients with septic shock, on days 1 and 4 of treatment. Twenty healthy adults were enrolled as a control group. Plasma SDC-1 content, serum VAP-1 activity, platelets, and leukocyte count were measured in septic shock group at baseline and at 72 h and compared with those of healthy controls.
VAP-1 activity and SDC-1 content were significantly increased in septic patients' group (P < 0.01) in comparison with controls. VAP-1 activity and SDC-1 content correlated positively to each other, and negatively to platelet count. In the septic shock group SDC-1 correlated on day 1 to SOFA score.
We found increased VAP-1 activity and SDC-1 content in critically ill patients with septic shock. Based on our results, the role of VAP-1 in shock pathogenesis should be studied with semicarbazide-sensitive amine oxidase activity blocking agents and substrate affinity testing.
2012. Vol. 56, no 3, 316-322 p.