This review summarizes the mechanistic role of nitric oxide, guanylate cyclase, and potassium channels in mediating the profound fall in peripheral vascular tone during sepsis and septic shock.
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Highlights potential targets for vasodilation reversal in sepsis; leaves open clinical translation pending randomized evidence.
Sepsis and septic shock are major causes of morbidity and mortality in critically ill patients. Sepsis and septic shock induce a profound fall in the peripheral vascular tone. NO has been implicated as a key player in vascular changes of sepsis and septic shock. In this brief review, two points are focused in greater detail: first, the involvement of guanylate cyclase and potassium channels in NO vascular effects in sepsis; second, the role played by NO and its two effectors in the long-lasting modifications of vascular reactivity in sepsis. Some recent developments in the area are reviewed.
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Fernandes et al. (2008) studied this question.
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