title: Sepsis-induced degradation of endothelial glycocalix.
abstract: Sepsis, a general inflammatory response to microbiological infection, is still a major cause of high mortality rates in intensive care units. This mortality rate strongly correlates with sepsis-induced impairment of organ blood supply as a consequence of disturbed capillary circulation and vascular leakage. Within this pathophysiological process, endothelial cell function plays a key role. Recent studies provide evidence that degradation of the glycocalix on the luminal cell membrane is an early step in septic vascular endothelial cell disorder and its shed compounds, such syndecan-1, heparan sulfate, intercellular-adhesion-molecule-1 (ICAM-1), and vascular-cell-adhesion-molecule-1 (VCAM-1), can be quantified in the plasma. The plasma concentrations of heparan sulfate and syndecan-1 strongly correlate with severity of sepsis and with inflammatory markers such as interleukin-6 (IL-6). Furthermore, a nonspecific deterioration of the glycocalix occurs during major abdominal surgery and during ischemia/reperfusion after vascular surgery. Both surgical treatments cause vascular leakage and, consequently, tissue edema, similar to that triggered by inflammatory impairment of the endothelial cell barrier. So far, no specific therapeutic strategies exist to maintain glycocalix integrity; hence, conserving endothelial function. Detection of glycocalix compounds in the plasma can be utilized as diagnostic markers to evaluate sepsis-induced endothelial damage and to estimate severity of sepsis. In the future, efforts will be made to prevent glycocalix damage during sepsis or major surgery. As a result, this will possibly preserve organ function and improve patient outcome.
authors.affiliation: Department of Anesthesiology, Intensive Care Medicine and Pain Therapy, Justus-Liebig-University Giessen, Germany. michael.henrich@anatomie.med.uni-giessen.de
authors.forename: Michael
authors.initials: M
authors.lastname: Henrich
authors.forename: Marco
authors.initials: M
authors.lastname: Gruss
authors.forename: Markus A
authors.initials: MA
authors.lastname: Weigand
mesh_terms: D004730:Endothelium, Vascular / Q000378:metabolism*; D019276:Glycocalyx / Q000378:metabolism*; D006801:Humans; D018805:Sepsis / Q000378:metabolism*