D-lactate as a marker of venous-induced intestinal ischemia: An experimental study in pigs

Background: Intestinal ischemia is difficult to diagnose. The search for biomarkers has led to an increased interest in D-lactate. D-lactate measured in higher concentrations arises from bacterial fermentation in the gastrointestinal tract. Permeable intestinal wall is an early consequence of intestinal ischemia, which allows D-lactate to enter the portal circulation. Methods: The superior mesenteric vein was clamped in eight pigs for two hours to induce ischemia of the intestine. Eight sham-operated pigs served as controls. Systemic and portal plasma D- and L-lactate, L-LDH and leukocytes were measured. Results: Plasma D-lactate increased significantly and nearly simultaneously in the systemic and portal circulation. After 75 min, samples from the jugular vein showed concentrations of .019 +/- .008 mmol/L in the sham group and .042 +/- .022 mmol/L in the intervention group (P = .023). A similar significant effect was seen in the portal circulation after 90 min. L-lactate increased five minutes after clamping in the portal circulation, with values of 3.396 + 1.119 mmol/L in the intervention group compared to 1.696 +/- .483 mmol/L in the control group (P = .006). L-LDH increased significantly in the intervention group, while leukocytes were unaffected. L-LDH and L-lactate in plasma led to an overestimation of D-lactate if not handled. Conclusion: Both systemic D- and L-lactate were markers of venous-induced intestinal ischemia. We speculate that D-lactate may be a valuable aid to the clinician in search of the anaerobic focus, because it may be more specific for mesenteric ischemia than L-lactate, in the sense that it is of bacterial origin. (C) 2011 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.