• Emiel Hendrik Post, Fuhong Su, Koji Hosokawa, Fabio Silvio Taccone, Antoine Herpain, Jacques Creteur, Jean-Louis Vincent, and Daniel De Backer.
• Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium.
• J. Surg. Res. 2017 Jan 1; 207: 145-154.

BackgroundThe etiology of renal dysfunction in sepsis is currently attributed to altered perfusion, microcirculatory abnormalities and cellular alterations. To clarify these mechanisms, we characterized the changes in renal perfusion and cortex metabolism in a large animal model of sepsis.MethodsWe studied 12 adult female sheep randomized to peritonitis-induced sepsis (n = 8) or to sham procedure (n = 4). A flow probe was positioned around the renal artery to measure renal blood flow (RBF). Laser Doppler was used to measure regional flow in the kidney cortex and medulla. A microdialysis probe was inserted into the renal cortex to measure cortical glucose, lactate, and pyruvate. Fluid resuscitation was provided to keep pulmonary artery occlusion pressure at baseline levels. All animals were observed for 18 h.ResultsHypotension occurred after 9 h in the septic animals (P = 0.02 versus baseline). RBF and cortical flow were significantly lower than at baseline from 12 h in the septic animals (P = 0.01 and P = 0.03, respectively). Cortical lactate and pyruvate levels increased in the septic animals from 3 and from 6 h, respectively (both P = 0.02 versus baseline), and the L/P ratio from 15 h (P = 0.01). There was a correlation between cortical flow and cortical L/P ratio after shock onset (r = -0.60, P = 0.002) but not before.ConclusionsIn this peritonitis model, sepsis was associated with metabolic alterations that may reflect early induction of cortical glycolysis. Septic shock was associated with reduced renal perfusion and decreased cortical and medullary blood flow, followed by signs of anaerobic metabolism in the cortex when flow reductions became critical.Copyright © 2016 Elsevier Inc. All rights reserved.

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