• José Gorrasi, Anestis Eleftheriadis, Jukka Takala, Sebastian Brandt, Siamak Djafarzadeh, Lukas E Bruegger, Hendrik Bracht, and Stephan M Jakob.
• Department of Intensive Care Medicine, University Hospital Bern (Inselspital), University of Bern, 3010 Bern, Switzerland.
• Biomed Res Int. 2013 Jan 1; 2013: 251084.

BackgroundChanges in hepatosplanchnic lactate exchange are likely to contribute to hyperlactatemia in sepsis. We hypothesized that septic and cardiogenic shock have different effects on hepatosplanchnic lactate exchange and its contribution to hyperlactatemia.Materials And Methods24 anesthetized pigs were randomized to fecal peritonitis (P), cardiac tamponade (CT), and to controls (n = 8 per group). Oxygen transport and lactate exchange were calculated during 24 hours.ResultsWhile hepatic lactate influx increased in P and in CT, hepatic lactate uptake remained unchanged in P and decreased in CT. Hepatic lactate efflux contributed 20% (P) and 33% (CT), respectively, to whole body venous efflux. Despite maintained hepatic arterial blood flow, hepatic oxygen extraction did not increase in CT.ConclusionsWhole body venous lactate efflux is of similar magnitude in hyperdynamic sepsis and in cardiogenic shock. Although jejunal mucosal pCO2 gradients are increased, enhanced lactate production from other tissues is more relevant to the increased arterial lactate. Nevertheless, the liver fails to increase hepatic lactate extraction in response to rising hepatic lactate influx, despite maintained hepatic oxygen consumption. In cardiac tamponade, regional, extrasplanchnic lactate production is accompanied by hepatic failure to increase oxygen extraction and net hepatic lactate output, despite maintained hepatic arterial perfusion.

32 keywords...

hide…