Under normal conditions endothelial cells form a metabolically active antithrombotic interface between blood and tissue by synthesizing numerous anticoagulant molecules such as glycosaminoglycans, thrombomodulin, nitric oxide, and prostacyclin. Following a hemostatic challenge, endothelial cells can substantially modify their behavior. Acute responses, epitomized by reactions to thrombin formation, include the rapid synthesis and secretion of mediators designed to assist in localizing and limiting the formation of a hemostatic plug (e.g. nitric oxide, prostacyclin). A series of slower-onset alterations in endothelial function take place, particularly on exposure to cytokines or bacterial endotoxins. These changes, which include expression of tissue factor, tend to render the endothelial surface more procoagulant. Such changes may be valuable when they occur locally, but could be detrimental if they take place systematically. This has led to the concept that therapy directed at antagonizing the effects of cytokines on the endothelium could be valuable in the critically ill patient.

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