[Pathophysiology of septic shock]

Antigen presentation to inflammatory cells via pattern recognition receptors leads to the synthesis of NF-kappaB and other cytokine transcriptional factors. Leukocytes in the blood bind to endothelial receptors, the expression of which is mediated by proinflammatory cytokines via leukocyte integrins; the leukocytes then migrate to the site of inflammation. Endothelial procoagulant activity during sepsis is partly responsible for the disseminated intravascular coagulation (DIVC) and tissue hypoperfusion that follow. The endothelium synthesizes numerous proinflammatory factors, including nitric oxide, which is responsible for the resistance acquired to endogenous catecholamines and for vasomotor paralysis. During sepsis, the autonomic nervous system activity decreases in favor of proinflammatory parasympathetic activity. Secretion of counterregulatory rather than proinflammatory hormones increases during sepsis. Organ dysfunctions may alter cell functions, essentially mitochondrial, as well as intertissue communication.