Nitric Oxide in Sepsis and Hemorrhagic Shock: Beneficial or Detrimental?

Controlling the inflammatory cascade, hemodynamic hemostasis, and cellular damage are of primary importance in treating and preventing organ failure and death associated with sepsis and hemorrhagic shock. The aim of this chapter is to explore the multifaceted means of regulation of Nitric Oxide (NO) and the inflammatory signals and secondary effects generated within sepsis and hemorrhagic shock. Specifically, NO mediated cGMP signaling, the immune response, and redox signaling. The pathophysiological roles of NO in sepsis and hemorrhagic shock will be presented with special attention on experimental data generated using pharmacological intervention for the modulation of inflammatory cytokines and hemodynamic change in animal or with human subjects when possible. The current therapy strategies of inhibiting NO production or scavenging excess NO in sepsis are reviewed.