d-Lactate is the dextrorotatory form of l-lactate. l-Lactate is the isomer routinely tested in clinical practice to assess cell hypoxemia. d-Lactate has been recently proposed as a specific marker of gut ischemia–reperfusion (IR), particularly after surgery for ruptured aortic aneurysms. We sought to assess d-lactate as a reliable marker of gut IR in a rat model of supraceliac aortic clamping.Design:
Prospective, randomized trial.Setting:
Animal research center.Subjects:
Male Wistar rats.Interventions:
After general anesthesia, rats were randomized into two groups (n = 8 in each). The IR group underwent a laparotomy, aortic clamping for 40 mins, and 1 hr of reperfusion. The control group underwent the same procedure, except for aortic clamping.Measurements and Main Results:
The following variables were tested after 1 hr of reperfusion (IR group) or after the equivalent time (control group): 1) tissue and cell insult via ileum morphometry and electron microscopy, serum glutamic transaminases (serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase), pH, and l-lactate; 2) systemic inflammatory response via tumor necrosis factor-α; and 3) d-lactate levels. After IR, mucous membrane thickness and villi height decreased significantly, respectively by 30% and 45%, and electron-microscopic examination showed typical IR mucous membrane cell insult. IR also caused lactic acidosis (pH = 7.16 ± 0.05 vs. 7.31 ± 0.02, p < .01; l-lactate = 7.1 ± 1.6 vs. 1.6 ± 0.4 mmol/L, p = .001) and increased blood levels of transaminases. Concurrently, the inflammatory response was characterized by an increase in tumor necrosis factor-α (213 ± 129 vs. 47 ± 32 pg/mL, p < .05). However, blood levels of d-lactate never increased after IR.Conclusions:
d-Lactate is not a reliable marker of gut IR in our model of supraceliac aortic clamping in rats.