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Liver Dysfunction: Nitric Oxide, Carbon Monoxide, and Reactive Oxygen Species

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Mechanisms of Organ Dysfunction in Critical Illness

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICMSOFT,volume 38))

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Abstract

The liver is regarded as both a mechanism and a target in the development of multiple organ failure (MOF) [1, 2]. Consequently, the characteristic features of this organ have to be taken into account to understand the pathways leading to its dysfunction. First, the blood supply to the liver is unique because it is fed by both the high pressure arterial (common hepatic) and the low pressure portal venous systems. The portal vein normally accounts for 75–80 % of total blood flow while the common hepatic artery contributes 20–25 %. Blood flow regulation is interdependent, in that changes in portal venous blood flow are compensated for by variations in hepatic arterial perfusion in order to maintain total organ blood flow. This phenomenon is often referred to as the hepatic arterial buffer response [3]. Second, because of its central synthetic rôle, changes in hepatic function cannot be ignored. Some of the numerous organ-specific metabolic pathways are highly oxygen dependent (e.g., gluconeogenesis and protein synthesis [4]). This is further underscored by intrahepatic metabolic compartmentation resulting from the different localization of metabolic activities within the periportal and perivenous regions [5].

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Radermacher, P., Matejovic, M., Brückner, U.B. (2002). Liver Dysfunction: Nitric Oxide, Carbon Monoxide, and Reactive Oxygen Species. In: Evans, T.W., Fink, M.P. (eds) Mechanisms of Organ Dysfunction in Critical Illness. Update in Intensive Care and Emergency Medicine, vol 38. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56107-8_21

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