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Role of Nitric Oxide in Sepsis and ADRS pp 283–297Cite as

Role of Nitric Oxide in Pulmonary Vascular Dysfunction

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Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 24))

Abstract

Early descriptions of patients with septic shock in which invasive monitoring was used emphasized the failure of a sustained response of the central venous pressure and cardiac output to volume replacement indicating pathological dilation of peripheral blood vessels [1]. Apart from the hemodynamic changes associated with shock, metabolic derangement and failure of multiple organ systems, including acute lung injury (ALI), were recorded in the majority of patients. Since early reports that a calcium-independent nitric oxide synthase (NOS) could be induced by endotoxin (LPS) and proinflammatory cytokines in extra-endothelial vascular tissue [2], considerable evidence(vide supra) has accumulated implicating nitric oxide (NO), derived from inducible iNOS, as a final mediator of sepsis-associated vasodilation and hyporesponsiveness to vasopressors. More recently, with the increasing awareness of the importance of oxygen delivery in determining the outcome of patients with sepsis, attention has focused on the regional distribution of blood flow both at an organ system and microcirculatory level. In this chapter, the evidence implicating the L-arginine/NO pathway as an important effector of sepsis-induced pulmonary vascular dysfunction is discussed.

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Authors
  1. M. J. D. Griffiths
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  2. T. W. Evans
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Editors and Affiliations

  1. Department of Surgery, Beth Israel Hospital, 330 Brookline Avenue, 02215, Boston, MA, USA

    M. P. Fink

  2. Department of Anesthesiology and Intensive Care, Lariboisière University Hospital, 2 rue Ambroise Paré, 75475, Paris Cedex 10, France

    Didier Payen

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Griffiths, M.J.D., Evans, T.W. (1995). Role of Nitric Oxide in Pulmonary Vascular Dysfunction. 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_18

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