Abstract
Septic shock is a severe systemic inflammatory response caused by infection with any of a wide variety of microorganisms. Clinically, it is characterized by fever, hypotension, and signs of organ hypoperfusion or dysfunction. The high mortality rate of septic shock, despite the administration of effective antimicrobial agents, fluids, and catecholamine vasopressors, has led to an extensive effort to identify the microbial products, host mediators, and cell- activation mechanisms that trigger and fuel the clinical manifestations of this syndrome. As a result of this effort, our understanding of septic shock has grown exponentially. However, although therapies targeting newly discovered pathogenic mechanisms have been developed, none have as yet demonstrated clinical efficacy [1], One of the most interesting mediators recently implicated in septic shock is nitric oxide (NO).
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Danner, R.L., Cobb, J., Van Dervort, A.L. (1995). Nitric Oxide as a Mediator of Hypotension and Inflammation in Sepsis. In: Fink, M.P., Payen, D. (eds) Role of Nitric Oxide in Sepsis and ADRS. Update in Intensive Care and Emergency Medicine, vol 24. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79920-4_11
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