BACKGROUND: The authors developed a microdialysis method for sampling lactate from the gut lumen to evaluate the metabolic state of the intestinal mucosa. The aim of the study was to evaluate the method in vivo during nonischemic systemic hyperlactatemia and gut ischemia. METHODS: Microdialysis capillaries were inserted in the lumen of jejunum, in the jejunal wall, 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 second experiment, 90 min of intestinal ischemia was induced by total (n = 6) or partial (n = 6) occlusion of the superior mesenteric artery followed by 60 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) to 0.50 (range, 0.15-1.18) and 0.86 (range, 0.35-2.05) mM. Total occlusion of superior mesenteric artery increased luminal lactate from a median of 0.09 (range, 0.06-0.17) to 2.37 (range, 1.29-2.98) and further up to 3.80 (range, 2.55-6.75) mM during reperfusion. Partial occlusion of superior mesenteric 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 superficial layers followed the arterial and mesenteric vein microdialysate lactate. CONCLUSIONS: Luminal lactate concentration, as measured by microdialysis, increases substantially during gut ischemia but does not respond to systemic hyperlactatemia per se. In contrast, gut wall microdialysis cannot distinguish between gut ischemia and systemic hyperlactatemia. Gut luminal microdialysis provides a method for the assessment of intestinal ischemia with a potential for clinical application.
BACKGROUND: The authors developed a microdialysis method for sampling lactate from the gut lumen to evaluate the metabolic state of the intestinal mucosa. The aim of the study was to evaluate the method in vivo during nonischemic systemic hyperlactatemia and gut ischemia. METHODS: Microdialysis capillaries were inserted in the lumen of jejunum, in the jejunal wall, 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 second experiment, 90 min of intestinal ischemia was induced by total (n = 6) or partial (n = 6) occlusion of the superior mesenteric artery followed by 60 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) to 0.50 (range, 0.15-1.18) and 0.86 (range, 0.35-2.05) mM. Total occlusion of superior mesenteric artery increased luminal lactate from a median of 0.09 (range, 0.06-0.17) to 2.37 (range, 1.29-2.98) and further up to 3.80 (range, 2.55-6.75) mM during reperfusion. Partial occlusion of superior mesenteric 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 superficial layers followed the arterial and mesenteric vein microdialysate lactate. CONCLUSIONS: Luminal lactate concentration, as measured by microdialysis, increases substantially during gut ischemia but does not respond to systemic hyperlactatemia per se. In contrast, gut wall microdialysis cannot distinguish between gut ischemia and systemic hyperlactatemia. Gut luminal microdialysis provides a method for the assessment of intestinal ischemia with a potential for clinical application.
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