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(Circulation. 2007;116:1896-1906.)
© 2007 American Heart Association, Inc.

Cardiovascular Surgery

Shedding of the Endothelial Glycocalyx in Patients Undergoing Major Vascular Surgery With Global and Regional Ischemia

Markus Rehm, MD; Dirk Bruegger, MD; Frank Christ, MD; Peter Conzen, MD; Manfred Thiel, MD; Matthias Jacob, MD; Daniel Chappell, MD; Mechthild Stoeckelhuber, PhD; Ulrich Welsch, MD, PhD; Bruno Reichart, MD; Klaus Peter, MD; Bernhard F. Becker, MD, PhD

From the Clinic of Anesthesiology (M.R., D.B., F.C., P.C., M.T., M.J., D.C., K.P.), Department of Anatomy (M.S., U.W.), Clinic of Cardiac Surgery (B.R.), and Department of Physiology (B.F.B.), Ludwig-Maximilians-University, Munich, Germany.

Correspondence to Dr Markus Rehm, Clinic of Anesthesiology, Ludwig-Maximilians University, Marchioninistrasse 15, 81377 Munich, Germany. E-mail markus.rehm{at}med.uni-muenchen.de

Received January 16, 2006; accepted August 22, 2007.

Background— The astonishing thickness of the endothelial glycocalyx, which rivals that of endothelial cells in the microvasculature, was disclosed in the last 15 years. As already demonstrated, this structure plays a key role in the regulation of inflammation and vascular permeability.

Methods and Results— Two components of the glycocalyx, syndecan-1 and heparan sulfate, were measured in arterial blood of 18 patients undergoing surgery of the ascending aorta with cardiopulmonary bypass (n=12 with and n=6 without deep hypothermic circulatory arrest) and of 14 patients undergoing surgery for infrarenal aortic aneurysm. Basal values of syndecan-1 (1.2 µg/dL) and heparan sulfate (590 µg/dL) of patients were similar to those of control subjects. Anesthesia and initiation of surgery caused no changes. Global ischemia with circulatory arrest (n=12) was followed by transient 42- and 10-fold increases in syndecan-1 and heparan sulfate, respectively, during early reperfusion (0 to 15 minutes). After regional ischemia of heart and lungs (cardiopulmonary bypass; n=6), syndecan-1 increased 65-fold, and heparan sulfate increased 19-fold. Infrarenal ischemia was followed by 15- and 3-fold increases, respectively (n=14). The early postischemic rises were positively correlated (r=0.76, P<0.001). Plasma concentrations of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 did not change. Circulating polymorphonuclear granulocytes and the level of postischemic heparan sulfate corresponded negatively. Immunohistochemical imaging and immunoassay of isolated hearts (guinea pig) substantiated syndecan-1 and heparan sulfate as components of the endothelial glycocalyx released into the coronary venous effluent. Electron microscopy revealed shedding of the glycocalyx after ischemia/reperfusion.

Conclusions— This study provides the first evidence in humans for shedding of the endothelial glycocalyx during ischemia/reperfusion procedures.

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CLINICAL PERSPECTIVE

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