d-lactate as a marker of venous-induced intestinal ischemia: an experimental study in pigs

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.

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.

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.

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.