Endothelial Cell Dysfunction in Septic Shock

Abstract

Sepsis is a life-threatening syndrome that represents the host systemic response to an inflammatory focus. The systemic inflammatory response is triggered when circulating neutrophils encounter the stimulus that results in their activation. When this response provokes hypotension and organ dysfunction, it is called septic shock. A large number of vascular abnormalities have been described in patients with septic shock. The endothelial cell layer which represents a very large area in contact with blood is tightly involved in these alterations. Injury to the vascular endothelium is a critical and early event in the acute inflammatory response in vivo. In the activated state, neutrophils express increased adhesive properties that allow them to bind to endothelial cells. The target, i.e, the endothelial cell, then becomes an active participant in the injury process. Indeed, many of the inflammatory mediators that induce activation in neutrophils also influence endothelial cells and change their physiology.