Conclusion
Over the last ten years or so, a role of NO in sepsis and MOF has been established. A number of studies have been performed in animals and in patients in which the generation of NO in sepsis has been pharmacologically manipulated. While improvements in hemodynamics have generally been reported, to date none of these investigations has clearly demonstrated improved organ function or outcomes in human sepsis.
It is becoming increasingly clear that NO mediates both cytoprotective and cytopathic roles in sepsis. However, much remains to be elucidated in terms of how NO mediates these effects and also whether the consequences of NO are causative or reactive to organ dysfunction. Future therapies, better targeted towards selectively inhibiting iNOS, will no doubt help to clarify this question. In addition, it is possible that targeting downstream effects of NO, such as mitochondrial dysfunction or promoting mitochondrial biogenesis, may emerge as possible approaches to the management of this complex and widespread condition.
Keywords
- Nitric Oxide
- Septic Shock
- Methylene Blue
- Mitochondrial Biogenesis
- Vasodilatory Shock
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Carré, J., Singer, M., Moncada, S. (2007). Nitric Oxide. In: Abraham, E., Singer, M. (eds) Mechanisms of Sepsis-Induced Organ Dysfunction and Recovery. Update in Intensive Care and Emergency Medicine, vol 44. Springer, Berlin, Heidelberg . https://doi.org/10.1007/3-540-30328-6_6
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