Intestinal Luminal Microdialysis

Tenhunen, Jyrki; Kosunen, H.; Alhava, Esko; Tuomisto, Leena; Takala, Jukka

doi:10.1097/00000542-199912000-00035

Cited by 69 publications

(22 citation statements)

References 25 publications

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“…More recent experiments have not shown increased vascular permeability in intestinal tissue under these conditions (Makley AT and Pritts TA, unpublished observations, 2011). Other studies have shown that sepsis- and coronary bypass surgery- induced changes in intraluminal rectal levels of lactic acid, a very small molecule compared with cytokine peptides, were not the result of lactate washout from the serum, except in cases of profound serum lactate elevation [36, 37]. In our present study, IL-6 serum levels were markedly elevated for a considerable period of time (at 1 and 3 h), and intraluminal IL-6 elevated at 6 h after shock could be a result of serum washout.…”

Section: Discussionmentioning

confidence: 99%

Hemorrhagic Shock Induces a Proinflammatory Milieu in the Gut Lumen

Sonnier¹,

Makley²,

Friend³

et al. 2011

Journal of Surgical Research

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Background Intestinal injury is a consequence of hemorrhagic shock and resuscitation. The intestinal mucosa has been shown to respond to ischemia/reperfusion injury with production of inflammatory mediators. Previous work in our laboratory indicates that intestinal epithelial cells secrete proinflammatory cytokines in the direction of both the lamina propria and intestinal lumen. The ability of the intestinal mucosa to transmit inflammatory signals into the gut lumen after hemorrhagic shock is unknown. We hypothesized that hemorrhagic shock results in secretion of proinflammatory cytokines into the gut lumen. Methods Male C57/Bl6 mice underwent femoral artery cannulation and hemorrhage to a systolic blood pressure of 20 mmHg for 1 h, then resuscitation with lactated Ringer’s (LR) solution. Sham animals were cannulated only. Mice were decannulated and sacrificed at intervals. Stool and succus were removed from intestinal segments, weighed, and placed into buffer solution. Specimens were analyzed via enzyme-linked immunosorbent assay (ELISA). Results Compared with sham-injured mice, hemorrhagic shock resulted in increased intestinal luminal cytokines. At 3 h after injury, elevated levels of IL-6 were found in the cecal stool. At 6 h after injury, TNFα, IL-6, and MIP-2 were significantly elevated in the cecal stool, and IL-6 and MIP-2 were significantly elevated in the distal colonic stool. Conclusions Hemorrhagic shock results in secretion of proinflammatory cytokines into the intestinal lumen. These findings suggest that the intestinal mucosa may transmit and receive signals in a paracrine fashion via the gut lumen.

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Section: Discussionmentioning

confidence: 99%

Hemorrhagic Shock Induces a Proinflammatory Milieu in the Gut Lumen

Sonnier¹,

Makley²,

Friend³

et al. 2011

Journal of Surgical Research

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“…Furthermore, several studies were able to show that a systemic lactate increase is actually a late consequence of acute mesenteric ischemia unless hypovolemia develops [10,34,35]. In similar studies, compromised mesenteric blood flow could not be detected by means of serum (arterial) lactate levels but rather by changes in the intramucosal carbon dioxide partial pressure [36], gastric intramucosal pH [37] and amount of intestinal luminal lactate [38,39,40]. Hence, numerous experimental studies also provided evidence that serum lactate is only sometimes elevated in very advanced acute mesenteric ischemia and is in general not helpful for diagnosing its early phase.…”

Section: Experimental Studies On Serum Lactate Levels In Acute Mesentmentioning

confidence: 99%

Beyond Lactate: Is There a Role for Serum Lactate Measurement in Diagnosing Acute Mesenteric Ischemia?

Demir

Ceyhan²,

Friess³

2012

Dig Surg

121

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Background/Aims: Measurement of serum lactate remains the most frequently applied laboratory investigation to diagnose acute mesenteric (intestinal) ischemia. The present review aims at critically questioning the widespread measurement of serum lactate to diagnose acute mesenteric ischemia in clinical practice and at drawing attention to more novel markers of intestinal ischemia. Methods: An electronic search of multiple databases was performed with the key words ‘lactate’, ‘marker’, ‘mesenteric’, ‘intestinal’ and ‘ischemia’ to detect all relevant studies. Additionally, the references of published articles were also reviewed. Results: Serum lactate is an unspecific marker of tissue hypoperfusion and undergoes significant elevation only after advanced mesenteric damage. While L-lactate is the routinely measured stereoisomer of lactate, the other stereoisomer, D-lactate, has been shown to bear a somewhat higher specificity, which is still not comparable to the extremely specific nature of ischemia markers from other organs (e.g. cardiac ischemia). Larger studies are currently lacking to reliably advocate the routine clinical usage of novel markers like mucosal damage markers such as intestinal fatty acid-binding protein. Conclusion: Based on current evidence, the level of no single serum marker, including serum lactate, is elevated early and specifically enough in the serum to diagnose acute mesenteric ischemia.

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“…Experimental trials suggest that the measurement of mucosal or intestinal luminal lactate by microdialysis is a valid method to investigate and depict intestinal ischemia [16,17]. Meanwhile, luminal equilibrium dialysis [11,12] is a feasible and non-invasive method for measurements rectal lactate in clinical research.…”

Section: Discussionmentioning

confidence: 99%

Luminal lactate in acute pancreatitis - validation and relation to disease severity

et al. 2012

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BackgroundIncreased rectal luminal lactate concentration may be associated with the severity of the septic shock and high dose of vasopressors. It suggests hypoperfusion of the gut mucosa. This is potentially associated with bacterial translocation from the gut leading to local and systemic inflammation. In acute pancreatitis (AP) bacterial translocation is considered as the key event leading to infection of necrotic pancreatic tissue and high severity of illness.MethodsWe used rectal luminal equilibration dialysis for the measurement of gut luminal lactate in 30 consecutive patients admitted to hospital due to acute pancreatitis to test the hypothesis that a single measurement of rectal luminal lactate predicts the severity of acute pancreatitis, the length of hospital stay, the need of intensive care and ultimately, mortality. We also tested the physiological validity of luminal lactate concentration by comparing it to luminal partial tension of oxygen. Additionally, a comparison between two different L-lactate analyzers was performed.ResultsHigh rectal luminal lactate was associated with low mucosal partial tension of oxygen (R = 0.57, p = 0.005) thereby indicating the physiological validity of the method. Rectal luminal lactate at the hospital admission was not associated with the first day or the highest SOFA score, CRP level, hospital length of stay, length of stay in intensive care or mortality. In this cohort of unselected consecutive patients with acute pancreatitis we observed a tendency of increased rectal lactate in the severe cases. Low precision and high bias was observed between two lactate analyzers.ConclusionsThe association between rectal luminal lactate and oxygen tension indicates that luminal lactate is a marker mucosal anaerobiosis. Comparison between two different analyzers showed poor, non-constant precision over the range of lactate concentrations. Rectal luminal lactate concentration at the time of hospital admission did not predict the severity of pancreatitis.

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Intestinal Luminal Microdialysis

Cited by 69 publications

References 25 publications

Hemorrhagic Shock Induces a Proinflammatory Milieu in the Gut Lumen

Hemorrhagic Shock Induces a Proinflammatory Milieu in the Gut Lumen

Beyond Lactate: Is There a Role for Serum Lactate Measurement in Diagnosing Acute Mesenteric Ischemia?

Luminal lactate in acute pancreatitis - validation and relation to disease severity

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