Central to the pathophysiology of sepsis and septic shock is an alteration in endothelial cell function and oxidative stress. Highly complex, integrated responses that include the activation of a number of cell types, inflammatory mediators and the hemostatic system are involved in endothelial dysfunction. On the other hand, the imbalance between the excessive production of reactive oxygen species and/or inadequate antioxidative defenses characterizes the oxidative stress. The overview of all these mechanisms suggests clinical biochemical markers as a possible therapeutic target together with correct intervention timing.