Endothelial dysfunction and interaction between inflammation and coagulation in sepsis and systemic inflammatory response syndrome (SIRS)

Pathophysiological mechanisms that are responsible for the development of systemic inflammatory response syndrome (SIRS), as well as sepsis, are extremely complex. They are based on the release of potent bioactive cytokines, chemokines, as well as on the activation of components of complement. All these complex reactions lead to certain changes in endothelium, and they also affect the regulation and lead to activation of coagulation (extrinsic and intrinsic pathway). They also activate the process of fibrinolysis which all contribute to coagulation abnormalities, and consequentially has impact on the development of multiple organ dysfunction. Endothelium is a bond between complex inflammatory reactions and activation of coagulation and it has a central role in activation and modification of haemostatic abnormalities during the systemic inflammation. Modification of inflammatory response by activation of coagulation also occurs by various mechanisms. These mechanisms include the reactions in which protease activated receptors, activated protein C, antithrombin and many other molecules are involved. The aim of this review is to illustrate the complex interaction between inflammation and coagulation with the focus on the significance of endothelium as the bond and the base of these complex reactions. The contribution of understanding and monitoring of coagulation activity parameters as well as biomarkers of endothelial dysfunction could find its place in potential new therapeutic approaches.