Figure 2.

The diagram shows the presumed context of pathophysiological processes with sepsis. With sepsis, the host response to infection leads to deregulation of the inflammatory response. This is characterised by elevated CRP and neopterin levels. At the same time, oxidative stress is deregulated by increased ROS and RNS production. An indicator of excessive NO production is an increased NOx level. Opposite antioxidation mechanisms are also activated: SOD catalyses the conversion of the superoxide radical to the less toxic and reactive hydrogen peroxide and ADMA competitively suppresses NO synthesis. The level of plasma antioxidant capacity can be determined as FRAP. Oxidative stress leads to cell damage by lipid peroxidation and nucleic acid damage. The level of these phenomena is described by MDA and 8-OHdG markers, respectively. Endothelial dysfunction also develops. Through the activation of the transcription factor KLF6 and subsequent MMP14 metalloproteinase, a massive release of soluble endoglin from the endothelium occurs. Its function in respect of sepsis has not yet been clearly identified. It is not clear whether it is only due to or causes endothelial dysfunction. Among other things, it increases the production of NO. Damage to membranes, nucleic acids and the endothelium, caused by oxidative stress, leads to tissue damage, subsequent organ dysfunction and the development of multiorgan failure. The level of organ dysfunction correlates to the mortality of patients who are in septic shock.