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Physiopathologie de la défaillance cardiaque

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Sepsis grave et choc septique

Part of the book series: Le point sur … ((POINT))

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Résumé

La dysfonction myocardique au cours du sepsis est une entité largement reconnue. Classiquement, elle débute dans les vingt-quatre heures ou dans les premiers jours du début du sepsis et se caractérise par une dépression de la fonction systolique (diminution de la fraction d’éjection) et une dilatation biventriculaire, surtout en cas d’apports liquidiens importants. Chez les survivants, la dépression myocardique évolue vers un retour à la normale au bout de cinq à sept jours. Au cours des dix à quinze dernières années, la généralisation de l’échocardiographie en réanimation a permis d’observer qu’en réalité, son expression clinique est très variable d’un sujet à l’autre et d’un moment à l’autre de l’évolution du choc septique. De ce fait, il semble plus approprié de parler de dysfonction que de dépression myocardique au cours du sepsis. D’un point de vue physiopathologique, il est probable que cette variabilité clinique traduise l’implication ou la prédominance de mécanismes différents. De très nombreux mécanismes potentiels ont en effet été démontrés. à l’extrême, en se fondant sur les travaux expérimentaux, on peut considérer que la totalité des voies de régulation des fonctions du cardiomyocyte sont altérées au cours du choc septique. De grandes incertitudes demeurent en fait sur le rôle réel de chacun des mécanismes proposés dans la littérature. On peut néanmoins distinguer des mécanismes extrinsèques aux myocytes cardiaques (surtout plasmatiques et/ ou endothéliaux), à effet souvent immédiat, et d’autres purement intramyocytaires, à effet volontiers plus retardé.

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Réfénces

  1. Jafri S, Lavine S, Field B et al. (1990) Left ventricular function in sepsis. Crit Care Med 18: 709–14

    Article  PubMed  CAS  Google Scholar 

  2. Jardin F, Valtier B, Beauchet A et al. (1994) Invasive monitoring combined with twodimensional echocardiographic study in septic shock. Intensive Care Med 20: 550–4

    Article  PubMed  CAS  Google Scholar 

  3. Poelaert J, Declerck C, Vogalaers D et al. (1997) Left ventricular systolic and diastolic function in septic shock. Intensive Care Med 23: 553–60

    Article  PubMed  CAS  Google Scholar 

  4. Munt B, Jue J, Gin K et al. (1998) Diastolic filling in human severe sepsis: an echocardiographic study. Crit Care Med 26: 1829–33

    Article  PubMed  CAS  Google Scholar 

  5. Jardin F, Fourme T, Page B et al. (1999) Persistent preload defect in severe sepsis despite fluid loading: a longitudinal echocardiographic study in patients with septic shock. Chest 116: 1354–9

    Article  PubMed  CAS  Google Scholar 

  6. Vieillard-Baron A, Caille V, Charron C et al. (2008) Actual incidence of global left ventricular hypokinesia in adult septic shock. Crit Care Med 36: 1701–6

    Article  PubMed  Google Scholar 

  7. Bouhemad B, Nicolas-Robin A, Arbelot C et al. (2009) Acute left ventricular dilatation and shock-induced myocardial dysfunction. Crit Care Med 37: 441–7

    Article  PubMed  Google Scholar 

  8. Etchecopar-Chevreuil C, François B, Clavel M et al. (2008) Cardiac morphological and functional changes during early septic shock: a transesophageal echocardiographic study. Intensive Care Med 34: 250–6

    Article  PubMed  Google Scholar 

  9. Bouhemad B, Nicola-Robin A, Arbelot C et al. (2008) Isolated and reversible impairment of ventricular relaxation in patients with septic shock. Crit Care Med 36: 766–74

    Article  PubMed  Google Scholar 

  10. Parker M, Shelhamer JSB (1984) Profound but reversible myocardial depression in patients with septic shock. Ann Int Med 100: 483–90

    Article  PubMed  CAS  Google Scholar 

  11. Parillo J (1990) Myocardial depression during septic shock in humans. Crit Care Med 18: 1183–4

    Article  Google Scholar 

  12. Hung J, Lew WY (1993) Temporal sequence of endotoxin-induced systolic and diastolic myocardial depression in rabbits. Am J Physiol 265: H810–9

    PubMed  CAS  Google Scholar 

  13. Tavernier B, Makhotine O, Lebuffe G et al. (1998) Systolic pressure variation as a guide to fluid therapy in patients with sepsis-induced hypotension. Anesthesiology 89: 1313–21

    Article  PubMed  CAS  Google Scholar 

  14. Sturgess DJ, Marwick TH, Joyce C et al. (2010) Prediction of hospital outcome in septic shock: a prospective comparison of tissue Doppler and cardiac biomarkers. Crit Care 14: R44

    Article  Google Scholar 

  15. Fernandes Jr C, Akamine N, Knobel E (1999) Cardiac troponin: a new serum marker of myocardial injury in sepsis. Intensive Care Med 25: 1165–8

    Article  PubMed  Google Scholar 

  16. Turner A, Tsamitros M, Bellomo R (1999) Myocardial cell injury in septic shock. Crit Care Med 27: 1775–80

    Article  PubMed  CAS  Google Scholar 

  17. Ver Elst K, Spapen H, Nguyen D et al. (2000) Cardiac Troponin I and T are biological markers of left ventricular dysfunction in septic shock. Clin Chem 46: 650–7

    Google Scholar 

  18. Kern H, Wittich R, Rohr U et al. (2001) Increased endothelial injury in septic patients with coronary artery disease. Chest 119: 874–83

    Article  PubMed  CAS  Google Scholar 

  19. Grocott-Mason R, Shah A (1998) Cardiac dysfunction in sepsis: new theories and clinical implications. Intensive Care Med 24: 286–95

    Article  PubMed  CAS  Google Scholar 

  20. Brett J, Gewrlach H, Nawroth P et al. (1989) Tumor necrosis factor/cachectin increases permeability of endothelial cell monolayer by a mechanism involving regulatory G proteins. J Exp Med 169: 1977–91

    Article  PubMed  CAS  Google Scholar 

  21. Ammann P, Fehr T, Minder E et al. (2001) Elevation of troponin I in sepsis and septic shock. Intensive Care Med 27: 965–9

    Article  PubMed  CAS  Google Scholar 

  22. Wu A (2001) Increased troponin in patients with sepsis and septic shock: myocardial necrosis or reversible myocardial depression? Intensive Care Med 27: 959–61

    Article  PubMed  CAS  Google Scholar 

  23. Hessel M, Atsma D, Van der Valk E et al. (2008) Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation. Eur J Physiol 455: 979–86

    Article  CAS  Google Scholar 

  24. Post F, Weilemann LS, Messow CM et al. (2008) B-type natriuretic peptide as a marker for sepsis-induced myocardial depression in intensive care patients. Crit Care Med 36: 3030–7

    Article  PubMed  CAS  Google Scholar 

  25. Pirracchio R, Deye N, Lukaszewicz AC et al. (2008) Impaired plasma B-type natriuretic peptide clearance in human septic shock. Crit Care Med 36: 2542–6

    Article  PubMed  CAS  Google Scholar 

  26. Parillo J (1989) The cardiovascular pathophysiology of sepsis. Ann Rev Med 40: 469–85

    Article  Google Scholar 

  27. Lefer A (1970) Role of a myocardial depressant factor in the pathogenesis of circulatory shock. Fed Proc 29: 1836–47

    PubMed  CAS  Google Scholar 

  28. Knuefermann P, Nemoto S, Baumgarten G et al. (2002) Cardiac inflammation and innate immunity in septic shock: is there a role for toll-like receptors? Chest 121: 1329–36

    Article  PubMed  CAS  Google Scholar 

  29. Nemoto S, Vallejo J, Knuefermann P et al. (1996) Escherichia coli LPS-induced LV dysfunction: role of toll-like receptor-4 in the adult heart. Am J Physiol 282: H2316–23

    Google Scholar 

  30. Zou L, Feng Y, Chen Y et al. (2010) Toll-like receptor 2 plays a critical role in cardiac dysfunction during polymicrobial sepsis. Crit Care Med 38: 1335–42

    PubMed  CAS  Google Scholar 

  31. Tavener SA, Long EM, Robbins SM et al. (2004) Immune cell toll-like receptor 4 is required for cardiac myocyte impairment during endotoxemia. Circ Res 95: 700–7

    Article  PubMed  CAS  Google Scholar 

  32. Tavener SA, Kubes P (2006) Cellular and molecular mechanisms underlying LPS-associated myocyte impairment. Am J Physiol Heart Circ Physiol 290: H800–6

    Article  PubMed  CAS  Google Scholar 

  33. Kumar A, Thota V, Dee L et al. (1996) Tumor necrosis factor alpha and interleukin 1 beta are responsible for in vitro myocardial cell depression induced by human septic shock serum. J Exp Med 183: 949–58

    Article  PubMed  CAS  Google Scholar 

  34. Joulin O, Petillot P, Labalette M et al. (2007) Cytokine profile of human septic shock serum inducing cardiomyocyte contractile dysfunction. Physiol Res 56: 291–7

    PubMed  CAS  Google Scholar 

  35. Finkel M, Oddis C, Jacob T et al. (1992) Negative inotropic Effects of cytokines on the heart mediated by nitric oxide. Science 257: 387–9

    Article  PubMed  CAS  Google Scholar 

  36. Kelly R, Balligand J, Smith T (1996) Nitric oxide and cardiac function. Circ Res 79: 363–80

    Article  PubMed  CAS  Google Scholar 

  37. Oral H, Dorn GW, Mann D (1997) Sphingosine mediates the immediate negative inotropic Effects of tumor necrosis factor-alpha in adult mammalian cardiac myocyte. J Biol Chem 272: 4836–42

    Article  PubMed  CAS  Google Scholar 

  38. Schreur K, Liu S (1997) Involvement of ceramide in inhibitory Effect of IL-1beta on L-type Ca2+ current in adult rat ventricular myocytes. Am J Physiol 272: H2591–8

    PubMed  CAS  Google Scholar 

  39. Kadokami T, McTiernan C, Kubota T et al. (2001) Effects of soluble TNF receptor treatment on lipopolysaccharide-induced myocardial cytokine expression. Am J Physiol 280: H2281–91

    CAS  Google Scholar 

  40. Haudek S, Spencer E, Bryant D et al. (1992) Overexpression of cardiac I-kB alpha prevents endotoxin-induced myocardial dysfunction. Am J Physiol 280: H962–8

    Google Scholar 

  41. Kumar A, Kumar A, Michael P et al. (2005) Human serum from patients with septic shock activates transcription factors STAT1, IRF1, and NF-?B and induces apoptosis in human cardiac myocytes. J Biol Chem 280: 42619–26

    Article  PubMed  CAS  Google Scholar 

  42. Jozefowicz E, Brisson H, Rozenberg S et al. (2007) Activation of peroxisome proliferatoractivated receptor-alpha by fenofibrate prevents myocardial dysfunction during endotoxemia in rats. Crit Care Med 35: 856–63

    Article  PubMed  CAS  Google Scholar 

  43. Dos Santos CC, Gattas DJ, Tsoporis JN et al. (2010) Sepsis-induced myocardial depression is associated with transcriptional changes in energy metabolism and contractile related genes: A physiological and gene expression-based approach. Crit Care Med 38: 894–902

    Article  PubMed  CAS  Google Scholar 

  44. Ramaciotti C, Sharkey A, McClellan G, Winegrad S (1992) Endothelial cells regulate cardiac contractility. Proc Natl Acad Sci 89: 471–80

    Article  Google Scholar 

  45. Shah A (1998) Paracrine modulation of heart cell function by endothelial cells. Cardivascular Res 31: 847–67

    Google Scholar 

  46. Mebazaa A, Mayoux E, Maeda K et al. (1993) Paracrine Effects of endocardial endothelial cells on myocyte contraction mediated via endothelin. Am J Physiol 265: H1841–6

    PubMed  CAS  Google Scholar 

  47. Mebazaa A, De Keulenaer G, Paqueron X et al. (2001) Activation of cardiac endothelium as a compensatory component in endotoxin-induced cardiomyopathy: role of endothelin, prostaglandins and nitric oxide. Circulation 104: 3137–44

    Article  PubMed  CAS  Google Scholar 

  48. Balligand J, Ungureanu-Longrois D, Simmons W et al. (1995) Induction of NO synthase in rat cardiac microvascular endothelium cells by IL-1beta and IFN-gamma. Am J Physiol 268: H1293–303

    PubMed  CAS  Google Scholar 

  49. Ungureanu-Longrois D, Balligand J, Okada J et al. (1995) Contractile responsiveness of ventricular myocytes to isoproterenol is regulate by induction of nitric oxide synthase activity in cardiac microvascular endothelial cells in heterotypic primary culture. Circ Res 77: 486–93

    Article  PubMed  CAS  Google Scholar 

  50. Shah A, MacCarthy P (2000) Paracrine and autocrine Effects of nitric oxide on myocardial function. Pharmacology & Therapeutics 86: 49–86

    Article  CAS  Google Scholar 

  51. Kirstein M, Rivet-Bastide M, Hatem S et al. (1995) Nitric oxide regulates the calcium current in isolated human atrial myocytes. J Clin Invest 95: 794–802

    Article  PubMed  CAS  Google Scholar 

  52. Flesch M, Kilter H, Cremers B et al. (1997) Acute Effect of nitric oxide and cyclic GMP on human myocardial contractility. J Pharmacol Exp 281: 1340–9

    CAS  Google Scholar 

  53. Paulus W, Vantrimpont P, Shah A (1994) Acute Effects of nitric oxide on left ventricular relaxation and diastolic distensibility in man. Circulation 89: 2070–8

    Article  PubMed  CAS  Google Scholar 

  54. Prendergast B, Sagach V, Shah A (1997) Basal release of nitric oxide augments the Frank-Starling response in isolated heart. Circulation 96: 1320–9

    Article  PubMed  CAS  Google Scholar 

  55. Corda S, Mebazaa A, Tavernier B et al. (1998) Paracrine regulation of cardiac myocytes in normal and septic heart. J Crit Care 13: 39–47

    Article  PubMed  CAS  Google Scholar 

  56. Rabuel C, Samuel J-L, Lortat-Jacob B et al. (2010) Activation of the ubiquitin proteolytic pathway in human septic heart and diaphragm. Cardiovascular Pathology 19: 158–64

    Article  PubMed  CAS  Google Scholar 

  57. Brady A, Poole-Wilson P, Harding S, Warren JB (1992) Nitric oxide production within cardiac myocytes reduces their contractility in endotoxemia. Am J Physiol 263: H1963–6

    PubMed  CAS  Google Scholar 

  58. Tavernier B, Li J, El-Omar M et al. (2001) Cardiac contractile impairment associated with increased phophorylation of troponin I in endotoxemic rats. FASEB J 15: 294–6

    PubMed  CAS  Google Scholar 

  59. Grover R, Zaccardelli D, Colice G et al. (1999) An open-label dose escalation study of the nitric oxide synthase inhibitor, N(G)-methyl-L-arginine hypochloride (546C88), in patients with septic shock. Glaxo Wellcome International Septic Shock Study Group. Crit Care Med 27: 913–22

    Article  PubMed  CAS  Google Scholar 

  60. Ichinose F, Buys ES, Neilan TG et al. (2007) Cardiomyocyte-specific overexpression of nitric oxide synthase 3 prevents myocardial dysfunction in murine models of septic shock. Circ Res 100: 130–9

    Article  PubMed  CAS  Google Scholar 

  61. Khadour F, Panas D, Ferdinandy P et al. (2002) Enhanced NO and superoxide generation in dysfunctional hearts from endotoxemic rats. Am J Physiol 283: H1108–15

    CAS  Google Scholar 

  62. Ferdinandy P, Danial H, Ambrus I et al. (2000) Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure. Circ Res 87: 241–7

    Article  PubMed  CAS  Google Scholar 

  63. Oyama J, Shimokawa H, Momii H et al. (1998) Role of nitric oxide and peroxynitrite in cytokine-induced sustained myocardial dysfunction in dogs in vivo. J Clin Invest 101: 2207–14

    Article  PubMed  CAS  Google Scholar 

  64. Ishida H, Ichimori K, Hirota Y et al. (1996) Peroxynitrite-induced cardiac myocytes injury. Free Radic Biol Med 20: 343–50

    Article  PubMed  CAS  Google Scholar 

  65. Lanone S, Mebazaa A, Heymes C et al. (2000) Muscular contractile failure in septic patients: role of the inductible nitric oxide synthase pathway. Am J Resp Crit Care Med 162: 2308–15

    Article  PubMed  CAS  Google Scholar 

  66. Wang W, Sawicki G, Schulz R (2002) Peroxynitrite-induced myocardial injury is mediated through matrix metalloproteinase-2. Cardiovascular Res 53: 165–74

    Article  CAS  Google Scholar 

  67. Iqbal M, Cohen R, Marzouk K, Liu S (2002) Time course of nitric oxide, peroxynitrite, and antioxidants in the endotoxemic heart. Crit Care Med 30: 1291–6

    Article  PubMed  CAS  Google Scholar 

  68. Lew W, Yasuda S, Yuan T, Hammond HK (1996) Endotoxin-induced cardiac depression is associated with decreased cardiac dihydropyridine receptors in rabbits. J Mol Cell Cardiol 28: 1367–71

    Article  PubMed  CAS  Google Scholar 

  69. Stengl M, Bartak F, Sykora R et al. (2010) Reduced L-type calcium current in ventricular myocytes from pigs with hyperdynamic septic shock. Crit Care Med 38: 579–87

    Article  PubMed  CAS  Google Scholar 

  70. Abi Gerges N, Tavernier B, Mebazaa A et al. (1999) Sequential changes in autonomic regulation of cardiac myocytes after in vivo endotoxin injection in rat. Am J Resp Crit Care Med 160: 1196–204

    Article  PubMed  CAS  Google Scholar 

  71. Dong L, Wu L, Ji Y, Liu M (2001) Impairment of the ryanodine-sensitive calcium release channels in the cardiac sarcoplasmic reticulum and it underlying mechanism during the hypodynamic phase of sepsis. Shock 16: 33–9

    Article  PubMed  CAS  Google Scholar 

  72. Ziolo M, Katoh H, Bers D (2001) Expression of inducible nitric oxide synthase depresses beta-adrenergic-stimulated calcium release from the sarcoplasmic reticulum in intact ventricular myocytes. Circulation 104: 2961–6

    Article  PubMed  CAS  Google Scholar 

  73. Zhu X, Bernecker OY, Manohar NS et al. (2005) Increased leakage of sarcoplasmic reticulum Ca2+ contributes to abnormal myocyte Ca2+ handling and shortening in sepsis. Crit Care Med 33: 598–604

    Article  PubMed  Google Scholar 

  74. Hassoun SM, Marechal X, Montaigne D et al. (2008) Prevention of endotoxin-induced sarcoplasmic reticulum calcium leak improves mitochondrial and myocardial dysfunction. Crit Care Med 36: 2590–6

    Article  PubMed  CAS  Google Scholar 

  75. Wu L, Ji Y, Dong L, Liu M (2001) Calcium uptake by sarcoplasmic reticlum is impaired during the hypodynamic phase of sepsis in the rat heart. Shock 15: 49–55

    PubMed  CAS  Google Scholar 

  76. Neviere R, Hassoun M, Decoster B et al. (2010) Caspase-dependent protein phosphatase 2A activation contributes to endotoxin-induced cardiomyocyte contractile dysfunction. Crit Care Med 38: 2031–6

    PubMed  CAS  Google Scholar 

  77. Tavernier B, Garrigue D, Boulle C et al. (1998) Myofilament calcium sensitivity is decreased in skinned cardiac fibers of endotoxinic-treated rabbits. Cardivascular Res 38: 472–9

    Article  CAS  Google Scholar 

  78. Tavernier B, Mebazaa A, Mateo P et al. (2001) Phosphorylation-dependent alteration in myofilament calcium sensitivity but normal mitochondrial function in septic heart. Am J Resp Crit Care Med 163: 362–7

    Article  PubMed  CAS  Google Scholar 

  79. Layland J, Cave AC, Warren C et al. (2005) Protection against endotoxemia-induced contractile dysfunction in mice with cardiac-specific expression of slow skeletal troponin I. FASEB J 19: 1137–9

    PubMed  CAS  Google Scholar 

  80. Marshall M, Anilkumar N, Layland J et al. (2009) Protein phosphatase 2A contributes to the cardiac dysfunction induced by endotoxemia. Cardiovasc Res 82: 67–76

    Article  PubMed  CAS  Google Scholar 

  81. Komukai K, Kurihara S (1997) Length-dependence of calcium-tension relationship in aequorin-injected ferret papillary muscles. Am J Physiol 273: H1068–74

    PubMed  CAS  Google Scholar 

  82. Lorts A, Burroughs T, Shanley T (2009) Elucidating the role of reversible protein phosphorylation in sepsis-induced myocardial dysfunction. Shock 32: 49–54

    Article  PubMed  CAS  Google Scholar 

  83. Jones S, Romano F (1990) Myocardial beta adrenergic receptor coupling to adenylate cyclase during developing septic shock. Circ Shock 30: 51–61

    PubMed  CAS  Google Scholar 

  84. Tang C, Liu M (1996) Initial externalization followed by internalization of beta-adrenergic receptors in rat heart during sepsis. Am J Physiol 270: R254–63

    Google Scholar 

  85. Wu L, Tang C, Liu M (1997) Hyper-and hypocardiodynamic states are associated with externalization and internalization, respectively, of alpha-adrenergic receptors in rat heart during sepsis. Shock 7: 318–22

    Article  PubMed  CAS  Google Scholar 

  86. Sulakhe P, Sandirasegrarane L, Davis J et al. (1996) Alterations in inotropy, nitric oxide and cyclic GMP synthesis, protein phosphorylation and ADP-ribosylation in the endotoxintreated rat myocardium and cardiomyocytes. Mol Cell Biochem 163/164: 305–18

    Article  CAS  Google Scholar 

  87. Reithmann C, Hallström S, Pilz G et al. (1993) Desensitization of rat cardiomyocyte adenylyl cyclase stimulation by plasma of noradrenaline-treated patients with septic shock. Circ Shock 41: 48–59

    PubMed  CAS  Google Scholar 

  88. Reithmann C, Gierschik P, Sidiropoulos D et al. (1989) Mechanism of noradrenalineinduced heterologous desensitization of adenylate cyclase stimulation in rat heart muscles cells: increase the level of inhibitory G-protein alpha-subunits. Eur J Pharmacol 172: 211–21

    Article  PubMed  CAS  Google Scholar 

  89. Moniotte S, Belge C, Sekkali B et al. (2007) Sepsis is associated with an upregulation of functional beta3 adrenoceptors in the myocardium. Eur J Heart Fail 9: 1163–71

    Article  PubMed  CAS  Google Scholar 

  90. Schmittinger CA, Wurzinger B, Deutinger M et al. (2010) How to protect the heart in septic shock: A hypothesis on the pathophysiology and treatment of septic heart failure. Medical Hypotheses 74: 460–5

    Article  PubMed  CAS  Google Scholar 

  91. Lee M, Hyun D, Jenner P, Halliwell B (2001) Effect of proteasome inhibition on cellular oxidative damage, antioxidant defences and nitric oxide production. J Neurochem 78: 32–41

    Article  PubMed  CAS  Google Scholar 

  92. Wu L, Tang C, Liu M (2001) Altered phosphorylation and calcium sensitivity of cardiac myofibrillar proteins during sepsis. Am J Physiol 281: R408–16

    Google Scholar 

  93. Fernandes Jr C, Iervolino M, Neves R et al. (1994) Interstitial myocarditis in sepsis. Am J Cardio 74: 958

    Article  Google Scholar 

  94. Larche J, Lancel S, Hassoun SM et al. (2006) Inhibition of mitochondrial permeability transition prever sepsis-induced myocardial dysfunction and mortality. J Am Coll Cardiol 48: 377–85

    Article  PubMed  CAS  Google Scholar 

  95. Singer M (2007) Powering up failed organs. Am J Respir Crit Care Med 176: 733–4

    Article  PubMed  Google Scholar 

  96. Brealey D, Brand M, Hargreaves I et al. (2002) Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet 360: 219–23

    Article  PubMed  CAS  Google Scholar 

  97. Brealey D, Rabuel C, Mebazaa A, Singer M (2002) iNOS expression and peroxynitrite productions is associated with mitochondrial dysfunction in skeletal muscle of patients with severe sepsis. Intensive Care Med 28: S17

    Google Scholar 

  98. Trumbeckaite S, Opalka J, Neuhof C et al. (2001) Different sensitivity of rabbit heart and skeletal muscle to endotoxin-induced impairment of mitochondrial function. Eur J Biochem 268: 1422–9

    Article  PubMed  CAS  Google Scholar 

  99. Panas D, Khadour F, Szabo C, Schulz R (1998) ProInflammatory cytokines depress cardiac efficiency by a nitric oxide-dependent mechanism. Am J Physiol 275: H1016–23

    PubMed  CAS  Google Scholar 

  100. Fauvel H, Marchetti P, Chopin C et al. (2001) Differential Effects of caspase inhibitors on endotoxin-induced myocardial dysfunction and heart apoptosis. Am J Physiol 280: H1608–14

    CAS  Google Scholar 

  101. Rudiger A, Singer M (2007) Mechanisms of sepsis-induced cardiac dysfunction. Crit Care Med 35: 1599–608

    Article  PubMed  Google Scholar 

  102. Lancel S, Joulin O, Favory R et al. (2005) Ventricular myocyte caspases are directly responsible for endotoxin-induced cardiac dysfunction. Circulation 111: 2596–604

    Article  PubMed  CAS  Google Scholar 

  103. Rozenberg S, Besse S, Brisson H et al. (2006) Endotoxin-induced myocardial dysfunction in senescent rats. Crit Care 10: R124

    Article  Google Scholar 

  104. Dyson A, Singer M (2009) Animal models of sepsis: Why does preclinical efficacy fail to translate to the clinical setting? Crit Care Med 37 (Suppl): S30–7

    Article  Google Scholar 

  105. Levy RJ, Piel DA, Acton PD et al. (2005) Evidence of myocardial hibernation in the septic heart. Crit Care Med 33: 2752–6

    Article  PubMed  Google Scholar 

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  3. A. Mebazaa
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Tavernier, B., Rabuel, C., Mebazaa, A. (2011). Physiopathologie de la défaillance cardiaque. In: Sepsis grave et choc septique. Le point sur …. Springer, Paris. https://doi.org/10.1007/978-2-8178-0064-6_3

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