Endothelial changes after shock and injury.

The endothelial cell (EC) was once though to be a passive bystander in the inflammatory response to shock and injury. We now know, however, that these cells play a central role in the coordination of the response to injury. Hypovolemic shock following traumatic injury initiates two primary mechanisms of cellular damage. These include ischemia/reperfusion injury and acute inflammation. The EC has four key functions that are altered by these states: a) control of coagulation, b) regulation of vascular tone, c) control of vascular permeability, and d) regulation of leukocyte adhesion and trafficking. In the settings of ischemia/reperfusion and acute inflammation, the EC takes on a proinflammatory phenotype and as such becomes prothrombotic, demonstrates enhanced vascular permeability, and becomes chemoattractant, facilitating leukocyte adhesion, activation, and migration. In this article, we explore each of the four EC functions in detail along with the alterations that occur when the proinflammatory phenotype becomes manifest. In addition, we elucidate novel therapeutic strategies that have arisen from this research.