- About this Journal ·
- Abstracting and Indexing ·
- Aims and Scope ·
- Annual Issues ·
- Article Processing Charges ·
- Author Guidelines ·
- Bibliographic Information ·
- Citations to this Journal ·
- Contact Information ·
- Editorial Board ·
- Editorial Workflow ·
- Free eTOC Alerts ·
- Publication Ethics ·
- Recently Accepted Articles ·
- Reviewers Acknowledgment ·
- Submit a Manuscript ·
- Subscription Information ·
- Table of Contents
BioMed Research International
Volume 2013 (2013), Article ID 251084, 8 pages
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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- B. Michaeli, A. Martinez, and J. P. Revelly, “Effects of endotoxin on lactate metabolism in humans,” Critical Care, vol. 16, article R139, 2012.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.