Endogenous Mediators in Sepsis and Septic Shock

Abstract

Publisher Summary The chapter introduces the pathogenesis of sepsis and various definitions of sepsis. The status of sepsis and cytokines are discussed wherein proinflammatory cytokines (TNF, interleukin-1, interleukin-8); anti-inflammatory cytokines (interleukin-6 and interleukin- 10); soluble TNF and IL-1 receptors, IL-2 receptor antagonists; and heat shock proteins (ischemia-reperfusion, ARDS, and multiple organ dysfunction syndrome) are described. The chapter also discusses two vasoactive agents, endothelin, and nitric oxide: NO and vascular hyporeactivity in sepsis, NO and myocardial contractility in sepsis, NO and myocardial contractility in sepsis, NO and experimental septic shock, and NO and clinical sepsis. Hemostasis in sepsis is also discussed in the chapter wherein the role of plasma cascade systems in sepsis (the coagulation system, the contact system, the fibrinolytic system, and the complement system) and the role of the endothelium in sepsis (endothelial cells as regulators of coagulation and therapeutic approaches to attenuate sepsis) are described. Various hormonal regulation—namely, stress hormones (hypothalamic-pituitary-adrenal axis, catecholamines and other stress hormones); fluid and electrolyte homeostasis (vasopressin, renin-angiotensin-aldosterone axis, and atrial natriuretic peptide); pituitary-thyroid axis; and reproductive axis are also discussed in the chapter. The interplay of mediators in sepsis is also presented.