• K Träger, A Brinkmann, M Georgieff, and P Radermacher.
• Sektion Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Universitätsklinik für Anästhesiologie, Universität Ulm. karl.traeger@medizin.uni-ulm.de
• Anaesthesist. 2000 May 1;49(5):451-4.

AbstractSepsis and SIRS are characterised by increased hepatosplanchnic blood flow and oxygen transport due to sepsis-associated hypermetabolism with enhanced oxygen uptake. Regional hypermetabolism may be linked with a mismatch of oxygen availability and demand potentially resulting in a pathological splanchnic oxygen uptake/supply dependency. Splanchnic hypermetabolism has been hypothesised to be due to increased hepatic gluconeogenesis caused by accelerated glucose precursor uptake resulting from increased release from the peripheral tissues. This increased precursor efflux is triggered by cytokines. The response of splanchnic haemodynamics and oxygen kinetics, however, to therapeutic interventions does not necessarily parallel the different metabolic pathways. Therefore, understanding of both tissue perfusion and oxygenation as well as metabolism is pivotal for evaluating the effects of different therapeutic strategies in intensive care medicine.

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