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BioMed Research International
Volume 2013 (2013), Article ID 251084, 8 pages
http://dx.doi.org/10.1155/2013/251084
Research Article

Different Contribution of Splanchnic Organs to Hyperlactatemia in Fecal Peritonitis and Cardiac Tamponade

1Department of Intensive Care Medicine, University Hospital Bern (Inselspital), University of Bern, 3010 Bern, Switzerland
2Department of Visceral Surgery and Medicine, University Hospital Bern (Inselspital), University of Bern, 3010 Bern, Switzerland

Received 30 April 2013; Revised 27 August 2013; Accepted 1 September 2013

Academic Editor: Stephen M. Pastores

Copyright © 2013 José Gorrasi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. J. Bakker, P. Gris, M. Coffernils, R. J. Kahn, and J.-L. Vincent, “Serial blood lactate levels can predict the development of multiple organ failure following septic shock,” American Journal of Surgery, vol. 171, no. 2, pp. 221–226, 1996. View at Publisher · View at Google Scholar · View at Scopus
  2. S. Trzeciak, R. P. Dellinger, M. E. Chansky et al., “Serum lactate as a predictor of mortality in patients with infection,” Intensive Care Medicine, vol. 33, no. 6, pp. 970–977, 2007. View at Publisher · View at Google Scholar · View at Scopus
  3. M. E. Mikkelsen, A. N. Miltiades, D. F. Gaieski et al., “Serum lactate is associated with mortality in severe sepsis independent of organ failure and shock,” Critical Care Medicine, vol. 37, no. 5, pp. 1670–1677, 2009. View at Publisher · View at Google Scholar · View at Scopus
  4. R. L. Chioléro, J.-P. Revelly, X. Leverve et al., “Effects of cardiogenic shock on lactate and glucose metabolism after heart surgery,” Critical Care Medicine, vol. 28, no. 12, pp. 3784–3791, 2000. View at Scopus
  5. A. Meregalli, R. P. Oliveira, and G. Friedman, “Occult hypoperfusion is associated with increased mortality in hemodynamically stable, high-risk, surgical patients,” Critical Care, vol. 8, no. 2, pp. R60–R65, 2004. View at Scopus
  6. S.-W. Lee, Y.-S. Hong, D.-W. Park et al., “Lactic acidosis not hyperlactatemia as a predictor of inhospital mortality in septic emergency patients,” Emergency Medicine Journal, vol. 25, no. 10, pp. 659–665, 2008. View at Publisher · View at Google Scholar · View at Scopus
  7. A. T. Maciel and M. Park, “Differences in acid-base behavior between intensive care unit survivors and nonsurvivors using both a physicochemical and a standard base excess approach: a prospective, observational study,” Journal of Critical Care, vol. 24, no. 4, pp. 477–483, 2009. View at Publisher · View at Google Scholar · View at Scopus
  8. C. Chrusch, C. Bands, D. Bose et al., “Impaired hepatic extraction and increased splanchnic production contribute to lactic acidosis in canine sepsis,” American Journal of Respiratory and Critical Care Medicine, vol. 161, no. 2, pp. 517–526, 2000. View at Scopus
  9. B. Michaeli, A. Martinez, and J. P. Revelly, “Effects of endotoxin on lactate metabolism in humans,” Critical Care, vol. 16, article R139, 2012.
  10. I. Giovannini, C. Chiarla, and G. Boldrini, “The relationship between oxygen extraction and venous pH in sepsis,” Shock, vol. 8, no. 5, pp. 373–377, 1997. View at Scopus
  11. S. E. Curtis and S. M. Cain, “Regional and systemic oxygen delivery/uptake relations and lactate flux in hyperdynamic, endotoxin-treated dogs,” American Review of Respiratory Disease, vol. 145, no. 2, pp. 348–354, 1992. View at Scopus
  12. D. C. Gore, F. Jahoor, J. M. Hibbert, and E. J. DeMaria, “Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability,” Annals of Surgery, vol. 224, no. 1, pp. 97–102, 1996. View at Publisher · View at Google Scholar · View at Scopus
  13. E. Ruokonen, J. Takala, A. Kari, H. Saxen, J. Mertsola, and E. J. Hansen, “Regional blood flow and oxygen transport in septic shock,” Critical Care Medicine, vol. 21, no. 9, pp. 1296–1303, 1993. View at Scopus
  14. M. Sair, P. J. Etherington, C. P. Winlove, and T. W. Evans, “Tissue oxygenation and perfusion in patients with systemic sepsis,” Critical Care Medicine, vol. 29, no. 7, pp. 1343–1349, 2001. View at Scopus
  15. S. M. Jakob, J. J. Tenhunen, S. Laitinen, A. Heino, E. Alhava, and J. Takala, “Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs,” American Journal of Physiology: Gastrointestinal and Liver Physiology, vol. 280, no. 5, pp. G819–G827, 2001. View at Scopus
  16. S. Brandt, T. Regueira, H. Bracht et al., “Effect of fluid resuscitation on mortality and organ function in experimental sepsis models,” Critical Care, vol. 13, no. 6, article R186, 2009. View at Publisher · View at Google Scholar · View at Scopus
  17. T. Regueira, S. Djafarzadeh, S. Brandt, et al., “Oxygen transport and mitochondrial function in porcine septic shock, cardiogenic shock, and hypoxaemia,” Acta Anaesthesiologica Scandinavica, vol. 56, pp. 846–859, 2012.
  18. S. M. Jakob, M. Merasto-Minkkinen, J. J. Tenhunen, A. Heino, E. Alhava, and J. Takala, “Prevention of systemic hyperlactatemia during splanchnic ischemia,” Shock, vol. 14, no. 2, pp. 123–127, 2000. View at Scopus
  19. D. Barthelmes, S. M. Jakob, S. Laitinen, S. Rahikainen, H. Ahonen, and J. Takala, “Effect of site of lactate infusion on regional lactate exchange in pigs,” British Journal of Anaesthesia, vol. 105, no. 5, pp. 627–634, 2010. View at Publisher · View at Google Scholar · View at Scopus
  20. J. M. Naylor, D. S. Kronfeld, D. E. Freeman, and D. Richardson, “Hepatic and extrahepatic lactate metabolism in sheep: effects of lactate loading and pH,” The American Journal of Physiology, vol. 247, no. 6, pp. E747–E755, 1984. View at Scopus
  21. M. Suistomaa, E. Ruokonen, A. Kari, and J. Takala, “Time-pattern of lactate and lactate to pyruvate ratio in the first 24 hours of intensive care emergency admissions,” Shock, vol. 14, no. 1, pp. 8–12, 2000. View at Scopus
  22. B. Levy, S. Gibot, P. Franck, A. Cravoisy, and P.-E. Bollaert, “Relation between muscle Na+K+ATPase activity and raised lactate concentrations in septic shock: a prospective study,” The Lancet, vol. 365, pp. 871–875, 2005.
  23. B. Levy, O. Desebbe, C. Montemont, and S. Gibot, “Increased aerobic glycolysis through β2 stimulation is a common mechanism involved in lactate formation during shock states,” Shock, vol. 30, no. 4, pp. 417–421, 2008. View at Publisher · View at Google Scholar · View at Scopus
  24. J. H. James, C.-H. Fang, S. J. Schrantz, P.-O. Hasselgren, R. J. Paul, and J. E. Fischer, “Linkage of aerobic glycolysis to sodium-potassium transport in rat skeletal muscle: implications for increased muscle lactate production in sepsis,” Journal of Clinical Investigation, vol. 98, no. 10, pp. 2388–2397, 1996. View at Scopus
  25. H. Bundgaard, K. Kjeldsen, K. Suarez Krabbe et al., “Endotoxemia stimulates skeletal muscle Na+ K+ ATPase and raises blood lactate under aerobic conditions in humans,” American Journal of Physiology: Heart and Circulatory Physiology, vol. 284, no. 3, pp. H1028–H1034, 2003. View at Scopus
  26. D. De Backer, J. Creteur, E. Silva, and J.-L. Vincent, “The hepatosplanchnic area is not a common source of lactate in patients with severe sepsis,” Critical Care Medicine, vol. 29, no. 2, pp. 256–261, 2001. View at Scopus
  27. M.-R. Losser, C. Bernard, J.-L. Beaudeux, C. Pison, and D. Payen, “Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits,” Journal of Applied Physiology, vol. 83, no. 5, pp. 1566–1574, 1997. View at Scopus
  28. R. Ding, D. Zhao, R. Guo, Z. Zhang, and X. Ma, “Treatment with unfractionated heparin attenuates coagulation and inflammation in endotoxemic mice,” Thrombosis Research, vol. 128, no. 6, pp. e160–e165, 2011. View at Publisher · View at Google Scholar · View at Scopus