Nitric oxide in septic shock.
Septic shock is a major cause of death following trauma and is a persistent problem in surgical patients throughout the world. It is characterised by hypotension and vascular collapse, with a failure of the major organs within the body. The role of excessive nitric oxide (NO) production, following the cytokine-dependent induction of the inducible nitric oxide synthase (iNOS), in the development of septic shock is discussed. Emphasis is placed upon the signal-transduction process by which iNOS is induced and the role of NO in cellular energy dysfunction and the abnormal function of the cardiovascular system and liver during septic shock.
D000818:Animals; D017209:Apoptosis; D004730:Endothelium, Vascular / Q000201:enzymology; D004790:Enzyme Induction; D006801:Humans; D008070:Lipopolysaccharides; D008099:Liver / Q000378:metabolism; D008956:Models, Chemical; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000737:chemistry; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D052247:Nitric Oxide Synthase Type II; D012772:Shock, Septic / Q000201:enzymology* / Q000209:etiology; D015398:Signal Transduction