Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia

Autores:: Caicedo, Juan Daniel
Diaztagle, Juan José
Navarrete Gutiérrez, Alejandro
Lamilla, Cesar Andrés
Ocampo Posada, Martín
Latorre Alfonso, Sergio Ivan
Alvarado, Jorge Iván
Cruz Martínez, Luis Eduardo

Tipo de recurso:: Article of journal

Fecha de publicación:: 2020

Institución:: Fundación Universitaria de Ciencias de la Salud - FUCS

Repositorio:: Repositorio Digital Institucional ReDi

Idioma:: spa

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dc.title.spa.fl_str_mv	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia
dc.title.translated.eng.fl_str_mv	The krebs cycle during sepsis and septic shock: a look at intermediate metabolism in hypoxia
title	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia
spellingShingle	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia ciclo de Krebs choque séptico hipoxia sepsis mitocondria Krebs cycle sepsis septic shock hypoxia mitochondria
title_short	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia
title_full	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia
title_fullStr	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia
title_full_unstemmed	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia
title_sort	Funcionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxia
dc.creator.fl_str_mv	Caicedo, Juan Daniel Diaztagle, Juan José Navarrete Gutiérrez, Alejandro Lamilla, Cesar Andrés Ocampo Posada, Martín Latorre Alfonso, Sergio Ivan Alvarado, Jorge Iván Cruz Martínez, Luis Eduardo
dc.contributor.author.spa.fl_str_mv	Caicedo, Juan Daniel Diaztagle, Juan José Navarrete Gutiérrez, Alejandro Lamilla, Cesar Andrés Ocampo Posada, Martín Latorre Alfonso, Sergio Ivan Alvarado, Jorge Iván Cruz Martínez, Luis Eduardo
dc.subject.spa.fl_str_mv	ciclo de Krebs choque séptico hipoxia sepsis mitocondria
topic	ciclo de Krebs choque séptico hipoxia sepsis mitocondria Krebs cycle sepsis septic shock hypoxia mitochondria
dc.subject.eng.fl_str_mv	Krebs cycle sepsis septic shock hypoxia mitochondria
publishDate	2020
dc.date.accessioned.none.fl_str_mv	2020-03-16 00:00:00 2022-06-29T19:38:09Z
dc.date.issued.none.fl_str_mv	2020-03-16
dc.date.available.none.fl_str_mv	2020-03-16 00:00:00 2022-06-29T19:38:09Z
dc.type.spa.fl_str_mv	Artículo de revista
dc.type.eng.fl_str_mv	Journal article
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dc.type.content.spa.fl_str_mv	Text
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dc.identifier.doi.none.fl_str_mv	10.31260/RepertMedCir.v29.n1.2020.969
dc.identifier.issn.none.fl_str_mv	0121-7372
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dc.identifier.eissn.none.fl_str_mv	2462-991X
dc.identifier.url.none.fl_str_mv	https://doi.org/10.31260/RepertMedCir.v29.n1.2020.969
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url	https://repositorio.fucsalud.edu.co/handle/001/2944 https://doi.org/10.31260/RepertMedCir.v29.n1.2020.969
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dc.relation.references.spa.fl_str_mv	Hotchkiss RS, Moldawer LL, Opal SM, Reinhart K, Turnbull IR, Vincent JL. Sepsis and septic shock. Nat Rev Dis Primers. 2016;2:16045. doi: 10.1038/nrdp.2016.45 2. Robin ED. Special report: dysoxia. Abnormal tissue oxygen utilization. Arch Intern Med. 1977;137(7):905-10. doi: 10.1001/archinte.137.7.905 3. Creery D, Fraser DD. Tissue dysoxia in sepsis: getting to know the mitochondrion. Crit Care Med. 2002;30(2):483-4. doi: 10.1097/00003246-200202000-00036 4. Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43(3):304-77. doi: 10.1007/s00134-017-4683-6. 5. Hernandez G, Teboul JL. Is the macrocirculation really dissociated from the microcirculation in septic shock?. Intensive Care Med. 2016;42(10):1621-4. doi: 10.1007/s00134-016-4416-2. 6. Ince C. Hemodynamic coherence and the rationale for monitoring the microcirculation. Crit Care. 2015;19 Suppl 3:S8. doi: 10.1186/cc14726 7. Hotchkiss RS, Rust RS, Dence CS, Wasserman TH, Song SK, Hwang DR, et al. Evaluation of the role of cellular hypoxia in sepsis by the hypoxic marker [18F]fluoromisonidazole. Am J Physiol. 1991;261(4 Pt 2):R965-72. doi: 10.1152/ajpregu.1991.261.4.R965 8. Groeneveld AB, van Lambalgen AA, van den Bos GC, Bronsveld W, Nauta JJ, Thijs LG. Maldistribution of heterogeneous coronary blood flow during canine endotoxin shock. Cardiovasc Res. 1991;25(1):80-8. doi: 10.1093/cvr/25.1.80 9. Abraham E, Singer M. Mechanisms of sepsis-induced organ dysfunction. Crit Care Med. 2007;35(10):2408-16. doi: 10.1097/01.ccm.0000282072.56245.91 10. Ospina-Tascon G, Neves AP, Occhipinti G, Donadello K, Buchele G, Simion D, et al. Effects of fluids on microvascular perfusion in patients with severe sepsis. Intensive Care Med. 2010;36(6):949-55. doi: 10.1007/s00134-010-1843-3. 11. Parrillo JE, Parker MM, Natanson C, Suffredini AF, Danner RL, Cunnion RE, et al. Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Ann Intern Med. 1990;113(3):227-42. doi: 10.7326/0003-4819-113-3-227 12. MacKenzie IM. The haemodynamics of human septic shock. Anaesthesia. 2001;56(2):130-44. doi: 10.1046/j.1365-2044.2001.01866.x 13. Court O, Kumar A, Parrillo JE. Clinical review: Myocardial depression in sepsis and septic shock. Crit Care. 2002;6(6):500-8. 14. Terborg C, Schummer W, Albrecht M, Reinhart K, Weiller C, Rother J. Dysfunction of vasomotor reactivity in severe sepsis and septic shock. Intensive Care Med. 2001;27(7):1231-4. doi: 10.1007/s001340101005 15. Aird WC. Endothelium and haemostasis. Hamostaseologie. 2015;35(1):11-6. doi: 10.5482/HAMO-14-11-0075. 16. Davis MJ. Perspective: physiological role(s) of the vascular myogenic response. Microcirculation. 2012;19(2):99-114. doi: 10.1111/j.1549-8719.2011.00131.x. 17.Trzeciak S, Cinel I, Phillip Dellinger R, Shapiro NI, Arnold RC, Parrillo JE, et al. Resuscitating the microcirculation in sepsis: the central role of nitric oxide, emerging concepts for novel therapies, and challenges for clinical trials. Acad Emerg Med. 2008;15(5):399-413. doi: 10.1111/j.1553-2712.2008.00109.x. 18. Chelazzi C, Villa G, Mancinelli P, De Gaudio AR, Adembri C. Glycocalyx and sepsis-induced alterations in vascular permeability. Crit Care. 2015;19:26. doi: 10.1186/s13054-015-0741-z 19. Price SA, Spain DA, Wilson MA, Harris PD, Garrison RN. Subacute sepsis impairs vascular smooth muscle contractile machinery and alters vasoconstrictor and dilator mechanisms. J Surg Res. 1999;83(1):75-80. doi: 10.1006/jsre.1998.5568 20. Marechal X, Favory R, Joulin O, Montaigne D, Hassoun S, Decoster B, et al. Endothelial glycocalyx damage during endotoxemia coincides with microcirculatory dysfunction and vascular oxidative stress. Shock. 2008;29(5):572-6. doi: 10.1097/SHK.0b013e318157e926. 21. Eichelbronner O, Sielenkamper A, Cepinskas G, Sibbald WJ, Chin-Yee IH. Endotoxin promotes adhesion of human erythrocytes to human vascular endothelial cells under conditions of flow. Crit Care Med. 2000;28(6):1865-70. doi: 10.1097/00003246-200006000-00030 22. Fink MP. Cytopathic hypoxia and sepsis: is mitochondrial dysfunction pathophysiologically important or just an epiphenomenon. Pediatr Crit Care Med 2015; 16: 89-91. doi: 10.1097/PCC.0000000000000299 23. Fink MP. Bench-to-bedside review: Cytopathic hypoxia. Crit Care. 2002;6(6):491-9. 24. Fink MP. Cytopathic Hypoxia Mitochondrial Dysfunction as Mechanism Contributing to Organ Dysfunction in Sepsis. Crit Care Clin 2001; 17(1): 219-237. 25. Levy RJ. Mit chondrial dysfunction, bioenergetic impairment, and metabolic down-regulation in sepsis. Shock. 2007;28(1):24-8. doi: 10.1097/01.shk.0000235089.30550.2d 26. Carré, J.E. & Singer, M. Cellular energetic metabolism in sepsis: the need for a systems approach. Biochim Biophys Acta 2008; 1777(7-8):763–771. doi: 10.1016/j.bbabio.2008.04.024 27. Levy B, Desebbe O, Montemont C, Gibot S. Increased aerobic glycolysis through beta2 stimulation is a common mechanism involved in lactate formation during shock states. Shock. 2008;30(4):417-21. doi: 10.1097/SHK.0b013e318167378f 28. Crouser ED, Julian MW, Blaho DV, Pfeiffer DR. Endotoxin-induced mitochondrial damage correlates with impaired respiratory activity. Crit Care Med. 2002;30(2):276-84. doi: 10.1097/00003246-200202000-00002 29. Eyenga P, Roussel D, Morel J, Rey B, Romestaing C, Teulier L, et al. Early septic shock induces loss of oxidative phosphorylation yield plasticity in liver mitochondria. J Physiol Biochem. 2014;70(2):285-96. doi: 10.1007/s13105-013-0280-5 30. Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol. 2004;287(3):502-16. doi: 10.1152/ajpregu.00114.2004 31. Taylor DE, Ghio AJ, Piantadosi CA. Reactive oxygen species produced by liver mitochondria of rats in sepsis. Arch Biochem Biophys. 1995;316(1):70-6. doi: 10.1006/abbi.1995.1011 32. Galley HF. Oxidative stress and mitochondrial dysfunction in sepsis. Br J Anaesth. 2011;107(1):57-64. doi: 10.1093/bja/aer093 33. Frayn KN, et al. Metabolic regulation. A human perspective. 3rd edn. 2010. Oxford: Willey Blackwell, 2010. 34. Connett RJ, Honig CR, Gayeski TE, Brooks GA. Defining hypoxia: a systems view of VO2, glycolysis, energetics, and intracellular PO2. J Appl Physiol (1985). 1990;68(3):833-42. doi: 10.1152/jappl.1990.68.3.833 35. Duke T. Dysoxia and lactate. Arch Dis Child. 1999;81(4):343-50. doi: 10.1136/adc.81.4.343 36. Hochachka PW. Oxygen, homeostasis, and metabolic regulation. Adv Exp Med Biol. 2000;475:311-35. doi: 10.1007/0-306-46825-5_30 37. Viollet B, Athea Y, Mounier R, Guigas B, Zarrinpashneh E, Horman S, et al. AMPK: Lessons from transgenic and knockout animals. Front Biosci (Landmark Ed). 2009;14:19-44. 38. Gomez H, Kellum JA, Ronco C. Metabolic reprogramming and tolerance during sepsis-induced AKI. Nat Rev Nephrol. 2017;13(3):143-51. doi: 10.1038/nrneph.2016.186. 39. Semenza GL, Wang GL. A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation. Mol Cell Biol. 1992;12(12):5447-54. doi: 10.1128/mcb.12.12.5447 40. Chandel NS, Maltepe E, Goldwasser E, Mathieu CE, Simon MC, Schumacker PT. Mitochondrial reactive oxygen species trigger hypoxia-induced transcription. Proc Natl Acad Sci U S A. 1998;95(20):11715-20. doi: 10.1073/pnas.95.20.11715 41. Poyton RO, Ball KA, Castello PR. Mitochondrial generation of free radicals and hypoxic signaling. Trends Endocrinol Metab. 2009;20(7):332-40. doi: 10.1016/j.tem.2009.04.001 42. Srivastava A, Mannam P. Warburg revisited: lessons for innate immunity and sepsis. Front Physiol 2015; 6: 70. doi: 10.3389/fphys.2015.00070 43. Senyilmaz D, Teleman AA. Chicken or the egg: Warburg effect and mitochondrial dysfunction. F1000Prime Rep. 2015;7:41. doi: 10.12703/P7-41 44. Solaini G, Baracca A, Lenaz G, Sgarbi G. Hypoxia and mitochondrial oxidative metabolism. Biochim Biophys Acta. 2010;1797(6-7):1171-7. doi: 10.1016/j.bbabio.2010.02.011 45. Kim JW, Tchernyshyov I, Semenza GL, Dang CV. HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia. Cell Metab. 2006;3(3):177-85. doi: 10.1016/j.cmet.2006.02.002 46. Nuzzo E, Berg KM, Andersen LW, Balkema J, Montissol S, Cocchi MN, et al. Pyruvate Dehydrogenase Activity Is Decreased in the Peripheral Blood Mononuclear Cells of Patients with Sepsis. A Prospective Observational Trial. Ann Am Thorac Soc. 2015;12(11):1662-6. doi: 10.1513/AnnalsATS.201505-267BC 47. Owen OE, Kalhan SC, Hanson RW. The key role of anaplerosis and cataplerosis for citric acid cycle function. J Biol Chem. 2002;277(34):30409-12. doi: 10.1074/jbc.R200006200 48. Randall HM, Jr., Cohen JJ. Anaerobic CO2 production by dog kidney in vitro. Am J Physiol. 1966;211(2):493-505. doi: 10.1152/ajplegacy.1966.211.2.493 49. Mullen AR, Wheaton WW, Jin ES, Chen PH, Sullivan LB, Cheng T, et al. Reductive carboxylation supports growth in tumour cells with defective mitochondria. Nature. 2011;481(7381):385-8. doi: 10.1038/nature10642 50. Chinopoulos C. Which way does the citric acid cycle turn during hypoxia? The critical role of alpha-ketoglutarate dehydrogenase complex. J Neurosci Res. 2013;91(8):1030-43. doi: 10.1002/jnr.23196 51. Pisarenko O, Studneva I, Khlopkov V, Solomatina E, Ruuge E. An assessment of anaerobic metabolism during ischemia and reperfusion in isolated guinea pig heart. Biochim Biophys Acta. 1988;934(1):55-63. doi: 10.1016/0005-2728(88)90119-3 52. Randle PJ, England PJ, Denton RM. Control of the tricarboxylate cycle and its interactions with glycolysis during acetate utilization in rat heart. Biochem J. 1970;117(4):677-95. doi: 10.1042/bj1170677 53. Weinberg JM, Venkatachalam MA, Roeser NF, Saikumar P, Dong Z, Senter RA, et al. Anaerobic and aerobic pathways for salvage of proximal tubules from hypoxia-induced mitochondrial injury. Am J Physiol Renal Physiol. 2000;279(5):F927-43. doi: 10.1152/ajprenal.2000.279.5.F927 54. Brekke E, Walls AB, Norfeldt L, Schousboe A, Waagepetersen HS, Sonnewald U. Direct measurement of backflux between oxaloacetate and fumarate following pyruvate carboxylation. Glia. 2012; 60(1): 147–158. doi: 10.1002/glia.21265 55. Hochachka PW, Dressendorfer RH. Succinate accumulation in man during exercise. Eur J Appl Physiol Occup Physiol. 1976;35(4):235-42. doi: 10.1007/bf00423282 56. Sanborn T, Gavin W, Berkowitz S, Perille T, Lesch M. Augmented conversion of aspartate and glutamate to succinate during anoxia in rabbit heart. Am J Physiol. 1979;237(5):H535-41. doi: 10.1152/ajpheart.1979.237.5.H535 57. Cerra FB, Siegel JH, Border JR, Peters DM, McMenamy RR. Correlations between metabolic and cardiopulmonary measurements in patients after trauma, general surgery, and sepsis. J Trauma. 1979;19(8):621-9. doi: 10.1097/00005373-197908000-00010 58. Whelan SP, Carchman EH, Kautza B, Nassour I, Mollen K, Escobar D, et al. Polymicrobial sepsis is associated with decreased hepatic oxidative phosphorylation and an altered metabolic profile. J Surg Res. 2014;186(1):297-303. doi: 10.1016/j.jss.2013.08.007 59. D’Alessandro A, Slaughter AL, Peltz ED, et al. Trauma/hemorrhagic shock instigates aberrant metabolic flux through glycolytic pathways, as revealed by preliminary 13C-glucose labeling metabolomics. J Transl Med 2015; 13: 253-265. doi: 10.1186/s12967-015-0612-z 60. Infantino V, Convertini P, Cucci L, Panaro MA, Di Noia MA, Calvello R, et al. The mitochondrial citrate carrier: a new player in inflammation. Biochem J. 2011;438(3):433-6. doi: 10.1042/BJ20111275 61. Selak MA, Armour SM, MacKenzie ED, Boulahbel H, Watson DG, Mansfield KD, et al. Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase. Cancer Cell. 2005;7(1):77-85. doi:: 10.1016/j.ccr.2004.11.022 62. Rubic T, Lametschwandtner G, Jost S, Hinteregger S, Kund J, Carballido-Perrig N, et al. Triggering the succinate receptor GPR91 on dendritic cells enhances immunity. Nat Immunol. 2008;9(11):1261-9. doi: 10.1038/ni.1657 63. Mills E, O'Neill LA. Succinate: a metabolic signal in inflammation. Trends Cell Biol. 2014;24(5):313-20. doi: 10.1016/j.tcb.2013.11.008
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spelling	Caicedo, Juan Danield9355a4053c9d07c924acbda480df7f9300Diaztagle, Juan José0d9fbed2aac05d2fee1293199a09eaa6Navarrete Gutiérrez, Alejandrob286dfd6a00d7e94e8cbf981435658df300Lamilla, Cesar Andrés9faee4d5701a063b96ab9df2c3dc5158300Ocampo Posada, Martín1bc7e4e9b627d3cb2e17f1230fff44c6300Latorre Alfonso, Sergio Ivan8c2ac6b901ecaf675ae91dcbceeb553b300Alvarado, Jorge Ivánc1a6301b314bdee3f05a95a6ea21a578300Cruz Martínez, Luis Eduardoae33b2793893338132765656a3f0dfb85002020-03-16 00:00:002022-06-29T19:38:09Z2020-03-162020-03-16 00:00:002022-06-29T19:38:09ZSociedad de Cirugía de Bogotá, Hospital de San José y Fundación Universitaria de Ciencias de la SaludRevista Repertorio de Medicina y Cirugía - 2020info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/http://purl.org/coar/access_right/c_abf2https://revistas.fucsalud.edu.co/index.php/repertorio/article/view/969ciclo de Krebschoque sépticohipoxiasepsismitocondriaKrebs cyclesepsisseptic shockhypoxiamitochondriaFuncionamiento del ciclo de krebs durante la sepsis y el choque séptico. Una mirada al metabolismo intermediario durante condiciones de hipoxiaThe krebs cycle during sepsis and septic shock: a look at intermediate metabolism in hypoxiaapplication/pdftext/htmlapplication/epub+ziptext/xmlaudio/mpegArtículo de revistaJournal articlehttp://purl.org/coar/resource_type/c_6501http://purl.org/coar/resource_type/c_dcae04bchttp://purl.org/coar/resource_type/c_2df8fbb1info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionTexthttp://purl.org/redcol/resource_type/ARTREVhttp://purl.org/coar/version/c_970fb48d4fbd8a8510.31260/RepertMedCir.v29.n1.2020.9690121-7372https://repositorio.fucsalud.edu.co/handle/001/29442462-991Xhttps://doi.org/10.31260/RepertMedCir.v29.n1.2020.969spaHotchkiss RS, Moldawer LL, Opal SM, Reinhart K, Turnbull IR, Vincent JL. Sepsis and septic shock. Nat Rev Dis Primers. 2016;2:16045. doi: 10.1038/nrdp.2016.45 2. Robin ED. Special report: dysoxia. Abnormal tissue oxygen utilization. Arch Intern Med. 1977;137(7):905-10. doi: 10.1001/archinte.137.7.905 3. Creery D, Fraser DD. Tissue dysoxia in sepsis: getting to know the mitochondrion. Crit Care Med. 2002;30(2):483-4. doi: 10.1097/00003246-200202000-00036 4. Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43(3):304-77. doi: 10.1007/s00134-017-4683-6. 5. Hernandez G, Teboul JL. Is the macrocirculation really dissociated from the microcirculation in septic shock?. Intensive Care Med. 2016;42(10):1621-4. doi: 10.1007/s00134-016-4416-2. 6. Ince C. Hemodynamic coherence and the rationale for monitoring the microcirculation. Crit Care. 2015;19 Suppl 3:S8. doi: 10.1186/cc14726 7. Hotchkiss RS, Rust RS, Dence CS, Wasserman TH, Song SK, Hwang DR, et al. Evaluation of the role of cellular hypoxia in sepsis by the hypoxic marker [18F]fluoromisonidazole. Am J Physiol. 1991;261(4 Pt 2):R965-72. doi: 10.1152/ajpregu.1991.261.4.R965 8. Groeneveld AB, van Lambalgen AA, van den Bos GC, Bronsveld W, Nauta JJ, Thijs LG. Maldistribution of heterogeneous coronary blood flow during canine endotoxin shock. Cardiovasc Res. 1991;25(1):80-8. doi: 10.1093/cvr/25.1.80 9. Abraham E, Singer M. Mechanisms of sepsis-induced organ dysfunction. Crit Care Med. 2007;35(10):2408-16. doi: 10.1097/01.ccm.0000282072.56245.91 10. Ospina-Tascon G, Neves AP, Occhipinti G, Donadello K, Buchele G, Simion D, et al. Effects of fluids on microvascular perfusion in patients with severe sepsis. Intensive Care Med. 2010;36(6):949-55. doi: 10.1007/s00134-010-1843-3. 11. Parrillo JE, Parker MM, Natanson C, Suffredini AF, Danner RL, Cunnion RE, et al. Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Ann Intern Med. 1990;113(3):227-42. doi: 10.7326/0003-4819-113-3-227 12. MacKenzie IM. The haemodynamics of human septic shock. Anaesthesia. 2001;56(2):130-44. doi: 10.1046/j.1365-2044.2001.01866.x 13. Court O, Kumar A, Parrillo JE. Clinical review: Myocardial depression in sepsis and septic shock. Crit Care. 2002;6(6):500-8. 14. Terborg C, Schummer W, Albrecht M, Reinhart K, Weiller C, Rother J. Dysfunction of vasomotor reactivity in severe sepsis and septic shock. Intensive Care Med. 2001;27(7):1231-4. doi: 10.1007/s001340101005 15. Aird WC. Endothelium and haemostasis. Hamostaseologie. 2015;35(1):11-6. doi: 10.5482/HAMO-14-11-0075. 16. Davis MJ. Perspective: physiological role(s) of the vascular myogenic response. Microcirculation. 2012;19(2):99-114. doi: 10.1111/j.1549-8719.2011.00131.x. 17.Trzeciak S, Cinel I, Phillip Dellinger R, Shapiro NI, Arnold RC, Parrillo JE, et al. Resuscitating the microcirculation in sepsis: the central role of nitric oxide, emerging concepts for novel therapies, and challenges for clinical trials. Acad Emerg Med. 2008;15(5):399-413. doi: 10.1111/j.1553-2712.2008.00109.x. 18. Chelazzi C, Villa G, Mancinelli P, De Gaudio AR, Adembri C. Glycocalyx and sepsis-induced alterations in vascular permeability. Crit Care. 2015;19:26. doi: 10.1186/s13054-015-0741-z 19. Price SA, Spain DA, Wilson MA, Harris PD, Garrison RN. Subacute sepsis impairs vascular smooth muscle contractile machinery and alters vasoconstrictor and dilator mechanisms. J Surg Res. 1999;83(1):75-80. doi: 10.1006/jsre.1998.5568 20. Marechal X, Favory R, Joulin O, Montaigne D, Hassoun S, Decoster B, et al. Endothelial glycocalyx damage during endotoxemia coincides with microcirculatory dysfunction and vascular oxidative stress. Shock. 2008;29(5):572-6. doi: 10.1097/SHK.0b013e318157e926. 21. Eichelbronner O, Sielenkamper A, Cepinskas G, Sibbald WJ, Chin-Yee IH. Endotoxin promotes adhesion of human erythrocytes to human vascular endothelial cells under conditions of flow. Crit Care Med. 2000;28(6):1865-70. doi: 10.1097/00003246-200006000-00030 22. Fink MP. Cytopathic hypoxia and sepsis: is mitochondrial dysfunction pathophysiologically important or just an epiphenomenon. Pediatr Crit Care Med 2015; 16: 89-91. doi: 10.1097/PCC.0000000000000299 23. Fink MP. Bench-to-bedside review: Cytopathic hypoxia. Crit Care. 2002;6(6):491-9. 24. Fink MP. Cytopathic Hypoxia Mitochondrial Dysfunction as Mechanism Contributing to Organ Dysfunction in Sepsis. Crit Care Clin 2001; 17(1): 219-237. 25. Levy RJ. Mit chondrial dysfunction, bioenergetic impairment, and metabolic down-regulation in sepsis. Shock. 2007;28(1):24-8. doi: 10.1097/01.shk.0000235089.30550.2d 26. Carré, J.E. & Singer, M. Cellular energetic metabolism in sepsis: the need for a systems approach. Biochim Biophys Acta 2008; 1777(7-8):763–771. doi: 10.1016/j.bbabio.2008.04.024 27. Levy B, Desebbe O, Montemont C, Gibot S. Increased aerobic glycolysis through beta2 stimulation is a common mechanism involved in lactate formation during shock states. Shock. 2008;30(4):417-21. doi: 10.1097/SHK.0b013e318167378f 28. Crouser ED, Julian MW, Blaho DV, Pfeiffer DR. Endotoxin-induced mitochondrial damage correlates with impaired respiratory activity. Crit Care Med. 2002;30(2):276-84. doi: 10.1097/00003246-200202000-00002 29. Eyenga P, Roussel D, Morel J, Rey B, Romestaing C, Teulier L, et al. Early septic shock induces loss of oxidative phosphorylation yield plasticity in liver mitochondria. J Physiol Biochem. 2014;70(2):285-96. doi: 10.1007/s13105-013-0280-5 30. Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol. 2004;287(3):502-16. doi: 10.1152/ajpregu.00114.2004 31. Taylor DE, Ghio AJ, Piantadosi CA. Reactive oxygen species produced by liver mitochondria of rats in sepsis. Arch Biochem Biophys. 1995;316(1):70-6. doi: 10.1006/abbi.1995.1011 32. Galley HF. Oxidative stress and mitochondrial dysfunction in sepsis. Br J Anaesth. 2011;107(1):57-64. doi: 10.1093/bja/aer093 33. Frayn KN, et al. Metabolic regulation. A human perspective. 3rd edn. 2010. Oxford: Willey Blackwell, 2010. 34. Connett RJ, Honig CR, Gayeski TE, Brooks GA. Defining hypoxia: a systems view of VO2, glycolysis, energetics, and intracellular PO2. J Appl Physiol (1985). 1990;68(3):833-42. doi: 10.1152/jappl.1990.68.3.833 35. Duke T. Dysoxia and lactate. Arch Dis Child. 1999;81(4):343-50. doi: 10.1136/adc.81.4.343 36. Hochachka PW. Oxygen, homeostasis, and metabolic regulation. Adv Exp Med Biol. 2000;475:311-35. doi: 10.1007/0-306-46825-5_30 37. Viollet B, Athea Y, Mounier R, Guigas B, Zarrinpashneh E, Horman S, et al. AMPK: Lessons from transgenic and knockout animals. Front Biosci (Landmark Ed). 2009;14:19-44. 38. Gomez H, Kellum JA, Ronco C. Metabolic reprogramming and tolerance during sepsis-induced AKI. Nat Rev Nephrol. 2017;13(3):143-51. doi: 10.1038/nrneph.2016.186. 39. Semenza GL, Wang GL. A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation. Mol Cell Biol. 1992;12(12):5447-54. doi: 10.1128/mcb.12.12.5447 40. Chandel NS, Maltepe E, Goldwasser E, Mathieu CE, Simon MC, Schumacker PT. Mitochondrial reactive oxygen species trigger hypoxia-induced transcription. Proc Natl Acad Sci U S A. 1998;95(20):11715-20. doi: 10.1073/pnas.95.20.11715 41. Poyton RO, Ball KA, Castello PR. Mitochondrial generation of free radicals and hypoxic signaling. Trends Endocrinol Metab. 2009;20(7):332-40. doi: 10.1016/j.tem.2009.04.001 42. Srivastava A, Mannam P. Warburg revisited: lessons for innate immunity and sepsis. Front Physiol 2015; 6: 70. doi: 10.3389/fphys.2015.00070 43. Senyilmaz D, Teleman AA. Chicken or the egg: Warburg effect and mitochondrial dysfunction. F1000Prime Rep. 2015;7:41. doi: 10.12703/P7-41 44. Solaini G, Baracca A, Lenaz G, Sgarbi G. Hypoxia and mitochondrial oxidative metabolism. Biochim Biophys Acta. 2010;1797(6-7):1171-7. doi: 10.1016/j.bbabio.2010.02.011 45. Kim JW, Tchernyshyov I, Semenza GL, Dang CV. HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia. Cell Metab. 2006;3(3):177-85. doi: 10.1016/j.cmet.2006.02.002 46. Nuzzo E, Berg KM, Andersen LW, Balkema J, Montissol S, Cocchi MN, et al. Pyruvate Dehydrogenase Activity Is Decreased in the Peripheral Blood Mononuclear Cells of Patients with Sepsis. A Prospective Observational Trial. Ann Am Thorac Soc. 2015;12(11):1662-6. doi: 10.1513/AnnalsATS.201505-267BC 47. Owen OE, Kalhan SC, Hanson RW. The key role of anaplerosis and cataplerosis for citric acid cycle function. J Biol Chem. 2002;277(34):30409-12. doi: 10.1074/jbc.R200006200 48. Randall HM, Jr., Cohen JJ. Anaerobic CO2 production by dog kidney in vitro. Am J Physiol. 1966;211(2):493-505. doi: 10.1152/ajplegacy.1966.211.2.493 49. Mullen AR, Wheaton WW, Jin ES, Chen PH, Sullivan LB, Cheng T, et al. Reductive carboxylation supports growth in tumour cells with defective mitochondria. Nature. 2011;481(7381):385-8. doi: 10.1038/nature10642 50. Chinopoulos C. Which way does the citric acid cycle turn during hypoxia? The critical role of alpha-ketoglutarate dehydrogenase complex. J Neurosci Res. 2013;91(8):1030-43. doi: 10.1002/jnr.23196 51. Pisarenko O, Studneva I, Khlopkov V, Solomatina E, Ruuge E. An assessment of anaerobic metabolism during ischemia and reperfusion in isolated guinea pig heart. Biochim Biophys Acta. 1988;934(1):55-63. doi: 10.1016/0005-2728(88)90119-3 52. Randle PJ, England PJ, Denton RM. Control of the tricarboxylate cycle and its interactions with glycolysis during acetate utilization in rat heart. Biochem J. 1970;117(4):677-95. doi: 10.1042/bj1170677 53. Weinberg JM, Venkatachalam MA, Roeser NF, Saikumar P, Dong Z, Senter RA, et al. Anaerobic and aerobic pathways for salvage of proximal tubules from hypoxia-induced mitochondrial injury. Am J Physiol Renal Physiol. 2000;279(5):F927-43. doi: 10.1152/ajprenal.2000.279.5.F927 54. Brekke E, Walls AB, Norfeldt L, Schousboe A, Waagepetersen HS, Sonnewald U. Direct measurement of backflux between oxaloacetate and fumarate following pyruvate carboxylation. Glia. 2012; 60(1): 147–158. doi: 10.1002/glia.21265 55. Hochachka PW, Dressendorfer RH. Succinate accumulation in man during exercise. Eur J Appl Physiol Occup Physiol. 1976;35(4):235-42. doi: 10.1007/bf00423282 56. Sanborn T, Gavin W, Berkowitz S, Perille T, Lesch M. Augmented conversion of aspartate and glutamate to succinate during anoxia in rabbit heart. Am J Physiol. 1979;237(5):H535-41. doi: 10.1152/ajpheart.1979.237.5.H535 57. Cerra FB, Siegel JH, Border JR, Peters DM, McMenamy RR. Correlations between metabolic and cardiopulmonary measurements in patients after trauma, general surgery, and sepsis. J Trauma. 1979;19(8):621-9. doi: 10.1097/00005373-197908000-00010 58. Whelan SP, Carchman EH, Kautza B, Nassour I, Mollen K, Escobar D, et al. Polymicrobial sepsis is associated with decreased hepatic oxidative phosphorylation and an altered metabolic profile. J Surg Res. 2014;186(1):297-303. doi: 10.1016/j.jss.2013.08.007 59. D’Alessandro A, Slaughter AL, Peltz ED, et al. Trauma/hemorrhagic shock instigates aberrant metabolic flux through glycolytic pathways, as revealed by preliminary 13C-glucose labeling metabolomics. J Transl Med 2015; 13: 253-265. doi: 10.1186/s12967-015-0612-z 60. Infantino V, Convertini P, Cucci L, Panaro MA, Di Noia MA, Calvello R, et al. The mitochondrial citrate carrier: a new player in inflammation. Biochem J. 2011;438(3):433-6. doi: 10.1042/BJ20111275 61. Selak MA, Armour SM, MacKenzie ED, Boulahbel H, Watson DG, Mansfield KD, et al. Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase. Cancer Cell. 2005;7(1):77-85. doi:: 10.1016/j.ccr.2004.11.022 62. Rubic T, Lametschwandtner G, Jost S, Hinteregger S, Kund J, Carballido-Perrig N, et al. Triggering the succinate receptor GPR91 on dendritic cells enhances immunity. Nat Immunol. 2008;9(11):1261-9. doi: 10.1038/ni.1657 63. Mills E, O'Neill LA. Succinate: a metabolic signal in inflammation. Trends Cell Biol. 2014;24(5):313-20. doi: 10.1016/j.tcb.2013.11.008https://revistas.fucsalud.edu.co/index.php/repertorio/article/download/969/1130https://revistas.fucsalud.edu.co/index.php/repertorio/article/download/969/1131https://revistas.fucsalud.edu.co/index.php/repertorio/article/download/969/1132https://revistas.fucsalud.edu.co/index.php/repertorio/article/download/969/1168https://revistas.fucsalud.edu.co/index.php/repertorio/article/download/969/1206Núm. 1 , Año 2020 : Enero - Abril129Revista Repertorio de Medicina y CirugíaPublicationOREORE.xmltext/xml3186https://repositorio.fucsalud.edu.co/bitstreams/9f577272-093c-417e-ae48-d300437f2523/download59b1a6000ab480c21eabdfb910abd73cMD51001/2944oai:repositorio.fucsalud.edu.co:001/29442024-02-02 13:11:51.333https://creativecommons.org/licenses/by-nc-sa/4.0/Revista Repertorio de Medicina y Cirugía - 2020metadata.onlyhttps://repositorio.fucsalud.edu.coRepositorio Digital de la Fundación Universitaria de Ciencias de la Saludredi@fucsalud.edu.co

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