Skip to main content

Volume 3 Supplement 1


Dexmedetomidine ameliorates gut lactate production and impairment of exogenous lactate clearance in an endotoxic sheep model


The mechanisms of persistent hyperlactemia during endotoxic shock are probably multifactorial. Both hypoperfusion-related anaerobic production and adrenergic-driven aerobic generation have been implicated. More recently an early and severe impairment in exogenous lactate clearance has also been described [1]. Theoretically, an excessive adrenergic response could influence all these mechanisms and thus aggravate the problem.


To assess the effects of dexmedetomidine (DEX) on lactate production and exogenous lactate clearance in an endotoxic shock model.


Twelve anesthetized sheep were subjected to a multimodal hemodynamic/perfusion assessment including hepatic and portal vein catheterizations, total hepatic blood flow, sublingual microcirculation, and muscle microdialysis. After the monitoring phase, all received a 5 mcg/kg LPS bolus (E coli O127:B8®) and then 4 mcg·kg1·hr1 for the rest of the experiment. After 1hr they were volume resuscitated, and then randomized to placebo or DEX. Sampling and exogenous lactate clearances [2] were performed at 4 points (figure 1).

figure 1

Figure 1


DEX was not associated with any adverse hemodynamic effect in terms of cardiac output, heart rate, mixed venous oxygen saturation, central venous-arterial pCO2 gradient and NE requirements as compared to placebo. DEX animals presented significant lower epinephrine levels (4.6 ± 1.3 vs 7.1 ± 1.4 ng/ml), arterial lactate levels (6.4 ± 3.1 vs 9.2 ± 1.8 mmol/l), portal vein lactate levels (6.2 ± 2.2 vs 8.1 ± 2.0 mmol/l); and higher portal vein O2 saturations (78 ± 16 vs 68 ± 11 %), and exogenous lactate clearance (7.2 ± 5.4 vs 2.9 ± 1.5 ml/kg/min) as compared to placebo at point D. No differences in muscle lactate production or sublingual microcirculatory parameters could be observed.


Dexmedetomidine ameliorates the increase in gut lactate production and impairment of exogenous lactate clearance in experimental endotoxic shock. This effect is associated with a significant reduction in systemic epinephrine levels.

Grant Acknowledgment

FONDECYT 1130200, Chile


  1. Tapia P, Soto D, Bruhn A, Regueira T, Jarufe N, Alegria L, et al: 0101. Early and severe impairment of lactate clearance in endotoxic shock is not related to liver hypoperfusion: preliminary report. Intensive Care Medicine Experimental. 2014, 2 (Suppl 1): P12

    Article  Google Scholar 

  2. Levraut J, Ciebiera JP, Chave S, Rabary O, Jambou P, Carles M, Grimaud D: Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J Respir Crit Care Med. 1998, 157: 1021-1026.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations


Rights and permissions

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Hernandez, G., Tapia, P., Ospina-Tascón, G. et al. Dexmedetomidine ameliorates gut lactate production and impairment of exogenous lactate clearance in an endotoxic sheep model. ICMx 3 (Suppl 1), A414 (2015).

Download citation

  • Published:

  • DOI: