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Serum heparan sulfate levels are elevated in endotoxemia

BACKGROUND: Increased vascular permeability is a characteristic feature of sepsis which, in the past, has been ascribed exclusively to a malfunction of endothelial cells. However, recently it has become evident that the endothelial glycocalyx is of considerable importance concerning various aspects...

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Detalles Bibliográficos
Autores principales: Hofmann-Kiefer, KF, Kemming, GI, Chappell, D, Flondor, M, Kisch-Wedel, H, Hauser, A, Pallivathukal, S, Conzen, P, Rehm, M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351938/
https://www.ncbi.nlm.nih.gov/pubmed/20149986
http://dx.doi.org/10.1186/2047-783X-14-12-526
Descripción
Sumario:BACKGROUND: Increased vascular permeability is a characteristic feature of sepsis which, in the past, has been ascribed exclusively to a malfunction of endothelial cells. However, recently it has become evident that the endothelial glycocalyx is of considerable importance concerning various aspects of vascular physiology, e.g. the vascular barrier and inflammation. Heparan sulfate, one of its essential components is characteristically traceable in blood, in case the endothelial glycocalyx is damaged or destroyed. METHODS: In 15 pigs we investigated whether the administration of endotoxin from gram-negative bacteria (Escherichia coli) results in increased serum levels of heparan sulfate, signalizing a shedding of the glycocalyx. In addition, markers of inflammation (white blood cell count, platelet count, tumour necrosis factor-α and interleukin-6) were evaluated over an observation period of 6 hours. RESULTS: Serum heparan sulfate concentrations significantly increased over time in the endotoxin group and were significantly elevated in comparison to the control group 6 hours after administration of endotoxin (p < 0.001). In the endotoxin group all markers of inflammation significantly changed during the time course. CONCLUSIONS: The administration of bacterial endotoxin induced a significant rise in degradation products of the endothelial glycocalyx.