Background: The authors developed a microdialysis method for sampling lacta
te from the gut lumen to evaluate the metabolic state of the intestinal muc
osa, The aim of the study was to evaluate the method in vivo during nonisch
emic systemic hyperlactatemia and gut ischemia.
Methods: Microdialysis capillaries were inserted in the lumen of jejunum, i
n the jejunal mall, and in the mesenteric artery and vein in anesthetized,
normoventilated pigs. In the first experiment, infusion of lactate was used
to clamp the arterial blood lactate at 5 mM and 10 mM (n = 6). In the seco
nd experiment, 90 min of intestinal ischemia was induced by total (n = 6) o
r partial (n = 6) occlusion of the superior mesenteric artery followed by 6
0 min of reperfusion, Sham-operated animals were used as controls (n = 6).
Results: Gut luminal lactate increased only slightly during the nonischemic
hyperlactatemia: from a median baseline value of 0.10 (range, 0.06-0.28) t
o 0.50 (range, 0.15-1.18) and 0.86 (range, 0.35-2.05) mM. Total occlusion o
f superior mesenteric artery increased luminal lactate from a median of 0.0
9 (range, 0.06-0.17) to 2.37 (range, 1.29-2.98) and further up to 3.80 (ran
ge, 2.55-6.75) mM during reperfusion. Partial occlusion of superior mesente
ric artery induced an increase from a median of 0.09 (range, 0.06-0.51) to
1.66 (range, 0.07-3.97) mM. Gut wall microdialysate lactate in deep and sup
erficial layers followed the arterial and mesenteric vein microdialysate la
ctate.
Conclusions: Luminal lactate concentration, as measured by microdialysis, i
ncreases substantially during gut ischemia but does not respond to systemic
hyperlactatemia per se. In contrast, gut mall microdialysis cannot disting
uish between gut ischemia and systemic hyperlactatemia. Gut luminal microdi
alysis provides a method for the assessment of intestinal ischemia with a p
otential for clinical application.