Abstract

Septic shock, a major clinical problem with mortality rates of up to 70%, is characterized by systemic hypotension, impaired tissue O2 extraction capabilities and myocardial depression. Nitric oxide (NO), a paracrine-acting gas enzymatically synthesized from L-arginine, is an important biologic mediator that has been implicated in the pathophysiologic alterations of septic shock. Endotoxin and cytokines such as tumor necrosis factor (TNF) or interferon-γ can induce the inducible form of NO synthase (NOS) in various cells, including macrophages, endothelial cells, vascular smooth muscle cells, or even myocardial cells. The resulting overproduction of inducible NO (iNOS) may exert deleterious hemodynamic effects including arterial hypotension [1]. vascular hyporeactivity and myocardial depression [2] and or directly induce cellular damage [3].

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