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Nitric Oxide Synthase Inhibition in Septic Shock

  • Conference paper
Yearbook of Intensive Care and Emergency Medicine 1994

Part of the book series: Yearbook of Intensive Care and Emergency Medicine 1994 ((YEARBOOK,volume 1994))

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Abstract

Severe sepsis is a common cause of morbidity and mortality in intensive care units [1]. When severe sepsis is associated with hypotension, the syndrome is called septic shock [2]. Depending on the subgroup of patients, mortality of septic shock ranges from 20 to 80%. Major characteristic of septic shock is cardiovascular dysfunction. The onset of septic shock is frequently associated with hypovolemia and hypotension. Fluid resuscitation often results in a hyperdynamic hemodynamic situation with low systemic vascular resistance, high cardiac output, and perpetuation of hypotension. Despite an elevated systemic oxygen delivery (DO2), maldistribution of blood flow and altered peripheral oxygen utilization contribute to cellular hypoxia, organ dysfunction, and fatal outcome. Manifold investigations suggest that excessive release of nitric oxide (NO) plays a major role in the pathogenesis of the hyperdynamic circulatory failure in septic shock.

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© 1994 Springer-Verlag Berlin Heidelberg

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Meyer, J., Hinder, F., Traber, D.L. (1994). Nitric Oxide Synthase Inhibition in Septic Shock. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1994. Yearbook of Intensive Care and Emergency Medicine 1994, vol 1994. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85068-4_8

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  • DOI: https://doi.org/10.1007/978-3-642-85068-4_8

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