medigraphic.com
A partir del año 2010, la Revista Oficial del INER cambió a NCT (Neumología y Cirugía de Tórax)

 Ver actualización

2009, Number 1

<< Back Next >>

Rev Inst Nal Enf Resp Mex 2009; 22 (1)

Mitochondrial dysfunction as possible cause of multiorgan failure associated to severe sepsis

Nava RHJ, Zamudio CP, Quiroz CY, Martínez RI, Espinosa PA, García CA, Domínguez DED

Language: Spanish
References: 38
Page: 37-47
PDF size: 141.22 Kb.


ABSTRACT

Sepsis is defined as an uncontrolled systemic inflammatory phenomenon and it is an important cause of morbidity and mortality all around the world. There are several important issues in the pathogenesis of septic phenomenon. First, the host response, more than the nature or type of infection, appears as a critical determinant in patient prognosis. Second, monocytes and endothelial cells play a central role in initiating and perpetuating the host response. Third, sepsis is clearly associated with the simultaneous activation of the inflammatory and coagulation cascades, and most of their components are markers or mediators of the host response. As corollary, the effort to defeat and eliminate pathogens may generate collateral damage on normal tissues, resulting in organ dysfunction and death. In the most exaggerated scenario, vasoregulatory dysfunction and microaggregation impair microvascular flow, creating local hypoxia, which may deteriorate cellular respiration. Impairment of oxygen delivery and utilization leads to global tissue hypoxia and mitochondrial respiration failure.


REFERENCES

  1. Schouten M, Wiersinga WJ, Levi M, van der Poll T. Inflammation, endothelium, and coagulation in sepsis. J Leukoc Biol 2008;83:536-545.

  2. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. N Engl J Med 2003;348:138-150.

  3. Briceño I. Sepsis: Definiciones y aspectos fisiopatológicos. Medicrit 2005;2:164-178.

  4. Gullo A, Iscra F, Di Capua G, et ál. Sepsis and organ dysfunction: an ongoing challenge. Minerva Anesthesiol 2005;71:671-699.

  5. Riedemann NC, Guo RF, Ward PA. Novel strategies for the treatment of sepsis. Nat Med 2003;9:517-524.

  6. Rodríguez TFA, Henao LAI, Osorno USC, Jaimes BFA. Guía de práctica clínica para el diagnóstico y tratamiento de la sepsis en el Servicio de Urgencias de Adultos. Iatreia 2007;20:223-243.

  7. Rivers EP, McIntyre L, Morro DC, Rivers KK. Early and innovative interventions for severe sepsis and septic shock: taking advantage of a window of opportunity. CMAJ 2005;173:1054-1065.

  8. Tomicic FV, Guerrero PJ. Endotelio y sepsis. Med Intensiva 2005;29:142-150.

  9. Hurtado BFJ, Nin VN, Rubbo AH. Estrés oxidativo y nitrosativo en la sepsis. Med Intensiva 2005;29:159-165.

  10. Taylor CT, Pouyssegur J. Oxygen, hypoxia, and stress. Ann N Y Acad Sci 2007;1113:87-94.

  11. Posadas CJG, Ugarte TA, Domínguez ChG. El transporte y la utilización tisular de oxígeno de la atmósfera a la mitocondria. Neumol Cir Torax 2006;65: 60-67.

  12. Ward J. Oxygen delivery and demand. Surgery (Oxford) 2006;24:354-360.

  13. Huang YC. Monitoring oxygen delivery in the critically ill. Chest 2005;128(5 Suppl 2):554S-560S.

  14. Treacher DF, Leach RM. Oxygen Transport-1. Basic Principles. BMJ 1998;317:1302-1306.

  15. Leach RM, Treacher DF. The pulmonary physician in critical care *2: oxygen delivery and consumption in the critically ill. Thorax 2002;57:170-177.

  16. Nathan AT, Singer M. The oxygen trail: tissue oxygenation. Br Med Bull 1999;5:96-108.

  17. Michiels C. Physiological and pathological responses to hypoxia. Am J Pathol 2004;164:1875-1882.

  18. Giaccia AJ, Simon MC, Johnson R. The biology of hypoxia: the role of oxygen sensing in development, normal function, and disease. Genes Dev 2004;18:2183-2194.

  19. Solaini G, Harris DA. Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion. Biochem J 2005;390(Pt 2):377-394.

  20. L´Her E, Sebert P. A global approach to energy metabolism in an experimental model of sepsis. Am J Respir Crit Care Med 2001;164(8 Pt 1):1444-1447.

  21. Navarro A, Boveris A. The mitochondrial energy transduction system and the aging process. Am J Physiol Cell Physiol 2007;292:C670-C686.

  22. Gottlieb RA. Mitochondria: execution central. FEBS Lett 2000;482:6-12.

  23. Pascual PP. Estudio de la muerte celular inmediata por reperfusión en cardiomiocitos en cultivo (tesis). Barcelona:Universidad Autónoma de Barcelona;2004.

  24. Duchen MR. Roles of mitochondria in health and disease. Diabetes 2004;53(Suppl 1):S96-S102.

  25. Gnaiger E, Lassnig B, Kuznetsov A, Rieger G, Margreiter R. Mitochondrial oxygen affinity, respiratory flux control and excess capacity of cytochrome C oxidase. J Exp Biol 1998;201(Pt 8):1129-1139.

  26. Jardines AA, Toledo CF. Alteraciones de la oxigenación en la sepsis severa. MEDISAN 2001;5:58-61.

  27. Pérez CR. La importancia de la energía en el estado de choque y sepsis. Rev Asoc Mex Med Crit Ter Int 2002;16:165-169.

  28. Fink MP. Bench-to-bedside review: cytopathic hypoxia. Crit Care 2002;6:491-499.

  29. Fink MP. Cytopathic hypoxia: is oxygen use impaired in sepsis as a result of an acquired intrinsic derangement in cellular respiration? Crit Care Clin 2002;18: 165-175.

  30. Bateman RM, Sharpe MD, Ellis CG. Bench-to-bedside review: microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide. Crit Care 2003;7:359-373.

  31. Callahan LA, Supinski GS. Sepsis induces diaphragm electron transport chain dysfunction and protein depletion. Am J Respir Crit Care Med 2005; 172:861-868.

  32. Crouser ED, Julian MW, Blaho DV, Pfeiffer DR. Endotoxin-induced mitochondrial damage correlates with impaired respiratory activity. Crit Care Med 2002; 30:276-284.

  33. Porta F, Takala J, Weikert C, et ál. Effects of prolonged endotoxemia on liver, skeletal muscle and kidney mitochondrial function. Crit Care 2006;10:R118.

  34. Brealey D, Brand M, Hargreaves I, et ál. Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet 2002;360:219-223.

  35. Crouser ED, Julian MW, Huff JE, et ál. Abnormal permeability of inner and outer mitochondrial membranes contributes independently to mitochondrial dysfunction in the liver during acute endotoxemia. Crit Care Med 2004;32:478-488.

  36. Pieczenik SR, Neustadt J. Mitochondrial dysfunction and molecular pathways of disease. Exp Mol Pathol 2007;83:84-92.

  37. Protti A, Singer M. Bench-to-bedside review: potential strategies to protect or reverse mitochondrial dysfunction in sepsis-induced organ failure. Crit Care 2006;10:228.

  38. Guzmán GAM, Velázquez GA, Sierra VMP. Óxido nítrico, estrés nitrosante y función mitocondrial. Rev Endocrinol Nutr 2006;14:227-232.




2020     |     www.medigraphic.com