Tenhunen J J, Kosunen H, Alhava E, Tuomisto L, Takala J A
Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Finland.
Anesthesiology. 1999 Dec;91(6):1807-15. doi: 10.1097/00000542-199912000-00035.
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.
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).
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.
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.
作者开发了一种用于从肠腔采集乳酸盐样本以评估肠黏膜代谢状态的微透析方法。本研究的目的是在非缺血性全身高乳酸血症和肠缺血期间对该方法进行体内评估。
将微透析毛细管插入麻醉状态下、通气正常的猪的空肠腔、空肠壁以及肠系膜动脉和静脉中。在第一个实验中，通过输注乳酸盐将动脉血乳酸盐浓度钳定在5 mM和10 mM（n = 6）。在第二个实验中，通过完全（n = 6）或部分（n = 6）阻断肠系膜上动脉诱导90分钟的肠缺血，随后进行60分钟的再灌注。假手术动物用作对照（n = 6）。
在非缺血性高乳酸血症期间，肠腔乳酸盐仅略有增加：从中位数基线值0.10（范围，0.06 - 0.28）增加到0.50（范围，0.15 - 1.18）和0.86（范围，0.35 - 2.05）mM。肠系膜上动脉完全阻断使肠腔乳酸盐从中位数0.09（范围，0.06 - 0.17）增加到2.37（范围，1.29 - 2.98），在再灌注期间进一步增加到3.80（范围，2.55 - 6.75）mM。肠系膜上动脉部分阻断导致从中位数0.09（范围，0.06 - 0.51）增加到1.66（范围，0.07 - 3.97）mM。深层和浅层肠壁微透析液中的乳酸盐与动脉和肠系膜静脉微透析液中的乳酸盐变化一致。
通过微透析测量的肠腔乳酸盐浓度在肠缺血期间显著增加，但本身对全身高乳酸血症无反应。相比之下，肠壁微透析无法区分肠缺血和全身高乳酸血症。肠腔微透析提供了一种评估肠缺血的方法，具有临床应用潜力。
