Currently there exists no reliable serum marker for the early diagnosis of acute mesenteric ischemia. We investigated D(—)‑lactate as a marker of acute mesenteric ischemia in a rat model. D(—)‑Lactate is a byproduct of bacterial metabolism; it is neither produced nor metabolized by mammalian cells. In an ischemic segment of bowel the resident microflora rapidly proliferate and soon overgrow the affected intestinal segment. Additionally, the mucosal barrier of the gut begins to break down. Under these conditions we hypothesize that D(—)‑lactate should cross the mucosal barrier in large quantities. To determine if this rapid bacterial proliferation and mucosal leakage produces D(—)‑lactate concentrations in quantities sufficient to elevate peripheral blood levels, two models of acute intestinal ischemia and one model of simple obstruction were developed in rats. The three models included: strangulation obstruction of terminal ileum, superior mesenteric artery ligation, and simple intestinal obstruction of the ileum. Controls were divided into two groups: sham-operated controls and unoperated controls. Serum samples were collected via an internal jugular catheter at 5 min, 2 hr, and 4 hr after surgery. These samples were then assayed for D(—)‑lactate using an enzymatic-spectrophotometric assay. Data was analyzed by repeated measures analysis of variance and where applicable the Student t test was used to determine statistical significance. We found statistically significant elevations in D(—)‑lactate concentrations as early as t = 5 min in the strangulation obstruction model and SMA ligation model compared to unoperated controls. At t = 2 hr as well as at t = 4 hr the SMA ligation model had significantly elevated levels compared to all groups. Additionally at t = 4 hr the ischemic obstruction model has significantly elevated levels compared to unoperated controls. We believe that the elevated D(—)‑lactate levels observed in the mesenteric ischemic models may be a useful marker of this disease in humans. © 1993 Academic Press, Inc.