To discuss a possible role of the endothelium in sepsis.
Studies published in biomedical journals and our own experimental results.
Studies on endothelial mechanisms in the context of sepsis.
Changes in endothelial cells on activation by inflammatory stimuli are reviewed briefly; potential mechanisms that lead to endothelial damage during sepsis are discussed.
The endothelium is a key organ involved in the pathogenesis of sepsis. Dysfunction of or injury to the endothelium may be involved in the pathogenesis of multiple organ failure and should be discriminated from activation resulting from stimulation with inflammatory stimuli. Identification of the molecular mechanisms that contribute to endothelial dysfunction or damage is likely to provide novel targets for the treatment of sepsis.
From the Central Laboratory of the Netherlands Red Cross Blood Transfusion Service (EH, SZ); the Department of Clinical Chemistry, Medical Center Vrije Universiteit, Amsterdam, The Netherlands (EH); and the Central Hematology Laboratory, Inselspital, Bern, Switzerland (SZ).
Presented, in part, at the Margaux Conference on Critical Illness, Margaux, France, November 8–12, 2000.
Endothelial dysfunction or injury may be the trigger for the development of multiple organ failure, yet the distinction between endothelial activation and endothelial dysfunction or damage is difficult to define in clinical sepsis.