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Changes in Cardiac Signal Transduction in Septic Shock

  • Conference paper
Yearbook of Intensive Care and Emergency Medicine

Part of the book series: Yearbook of Intensive Care and Emergency Medicine ((YEARBOOK,volume 1996))

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Abstract

Septic shock is the systemic response to serious infection and represents a predominant cause of death in intensive care [1]. Initiated by a local infection, bacteremia develops which is accompanied by a systemic distribution of bacterial toxins, leading to the activation of mediator cells such as granulocytes and macrophages, and frequently results in a lethal multiple organ failure (MOF) caused by these mediator substances and the bacterial toxins [2]. The invasion of mainly gram-negative bacteria is accompanied by fever as high as 41°C, vasodilatation, tachycardia, hyperventilation, and often mental disturbances. These clinical signs can be harbingers of manifest shock [3].

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References

  1. Wilson F (1984) Surgical intensive care units. In: Parillo JE, Ayres SM (eds) Major issues in critical care medicine. Williams & Wilkins, Baltimore, pp 17–33

    Google Scholar 

  2. Neuhof H (1989) Zur Rolle der Mediatoren bei Sepsis. Intensivmedizin 26 (Suppl1): 3–9

    Google Scholar 

  3. Weil MH, von Planta M, Rackow EC (1988) Acute circulatory failure. In: Braunwald E (ed) Heart disease. Saunders, Philadelphia, pp 575–576

    Google Scholar 

  4. Finland M (1970) Changing ecology of bacterial infections as related to antibacterial therapy. J Infect Dis 122:419–431

    Article  PubMed  CAS  Google Scholar 

  5. Parillo JE (1989) Septic shock in humans: Clinical evaluation, pathophysiology, and therapeutical approach. In: Shoemaker WC, Thompson WL, Holbrook P, et al (eds) Textbook of Critical Care. 2nd ed. Saunders, Philadelphia, pp 1006–1023

    Google Scholar 

  6. Ispahani P, Pearson NJ, Greenwood D (1963) An analysis of community- and hospitalacquired bacteraemia in a large teaching hospital in the United Kingdom. Quart J Med:427–440

    Google Scholar 

  7. Parker MM, Shelhammer JH, Natanson C, et al (1987) Serial cardiovascular variables in survivors and nonsurvivors of human septic shock: Heart rate as an early predictor of prognosis. Crit Care Med 15: 923–929

    Article  PubMed  CAS  Google Scholar 

  8. Werdan K, Boeksteger P, Müller U (1991) Akute septische Kardiomyopathie: Bestandteil der Multiorganversagen in der Sepsis? Med Klin 86: 526–534

    CAS  Google Scholar 

  9. Parillo JE (1989) The cardiovascular pathophysiology of sepsis. Ann Rev Med 40:469–485

    Article  Google Scholar 

  10. Parker MM, Shelhammer JH, Baccherach SL, et al (1984) Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med 100: 483–490

    PubMed  CAS  Google Scholar 

  11. Levinson MA, Tsao TC, Trunkey DD (1984) Myocardial depression. The effect of Ca + + and calcium flux during sepsis. Arch Surg 119: 803–808

    Google Scholar 

  12. Nishijima H, Weil MH, Shubin H, et al (1973) Hemodynamic and metabolic studies on shock associated with gram-negative bacteremia. Medicine 52: 287–293

    Article  PubMed  CAS  Google Scholar 

  13. Hallström S, Vogi C, Redl H, Schlag G (1990) Net inotropic plasma activity in canine hypovolemic traumatic shock: Low molecular weight plasma fraction after prolonged hypotension depresses cardiac muscle performance in vitro. Circ Shock 30: 129–144

    PubMed  Google Scholar 

  14. Bristow MR, Ginsburg R, Minobe W, et al (1982) Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. N Engl J Med 307: 205–211

    Article  PubMed  CAS  Google Scholar 

  15. Böhm M, Diet F, Feiler G, et al (1988) Subsensitivity of the failing human heart to isoprenaline and milrinone is related to [3-adrenoceptor downregulation. J Cardiovasc Pharm 12:726–732

    Article  Google Scholar 

  16. Böhm M, Gierschik P, Jakobs KH, et al (1990) Increase of Giα in human hearts with dilated but not ischemic cardiomyopathy. Circulation 82: 1249–1265

    Article  PubMed  Google Scholar 

  17. Weitzberg E, Lundberg JM, Rudehill A (1991) Elevated plasma levels of endothelin in patients with sepsis syndrome. Circ Shock 33: 222–227

    PubMed  CAS  Google Scholar 

  18. Conrad SA, Finkelstein JL, Madden MR, et al (1990) Cardiovascular dysfunction in multiple organ failure. In: Deitch Ed (ed) Multiple Organ Failure - Pathophysiology and Basic Concepts of Therapy. Thieme Inc, New York Stuttgart, pp 172–191

    Google Scholar 

  19. Böhm M, Kirchmayr R, Gierschik P, Erdmann E (1995) Increase of myocardial inhibitory G-proteins in catecholamine refractory septic shock or in septic multiorgan failure. Am J Med 98:183–186

    Article  PubMed  Google Scholar 

  20. Reithmann C, Gierschik P, Sidiropoulos D, et al (1989) Mechanism of noradrenalineinduced heterologous desensitisation of adenylate cyclase stimulation in rat heart muscle cells: Increase in the level of inhibitory G-protein α-subunits. Eur J Pharmacol (Mol Pharmacol) 172:211–221

    Article  CAS  Google Scholar 

  21. Reithmann C, Gierschik P, Werdan K, et al (1991) Tumor necrosis factor α upregulates Giα and Gβ proteins and adenylate cyclase responsiveness in rat cardiomyocytes. Eur J Pharmacol (Mol Pharmacol) 206: 53–60

    Article  CAS  Google Scholar 

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

    PubMed  CAS  Google Scholar 

  23. Suffredini AF, Fromm RE, Parker MM, et al (1989) The cardiovascular response of normal humans to the administration of endotoxin. N Engl J Med 321: 280–287

    Article  PubMed  CAS  Google Scholar 

  24. Carli A, Auclair MC, Benassaya C, Nunez E (1981) Evidence for an early lipid soluble cadiodepressant factor in rat serum after a sublethal dose of endotoxin. Circ Shock 8:301–312

    PubMed  CAS  Google Scholar 

  25. Moncada S, Palmer RMJ, Higgs EA (1991) Nitric oxide: Physiology, pathophysiology and pharmacology. Pharmacol Rev 43: 109–42

    PubMed  CAS  Google Scholar 

  26. De Belder AJ, Radomski MW, Why HJF, et al (1993) Nitric oxide synthase activities in human myocardium. Lancet 341: 84–85

    Article  PubMed  Google Scholar 

  27. Finkel MS, Oddis CV, Jacob TD, et al (1992) Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 257: 387–389

    Article  PubMed  CAS  Google Scholar 

  28. Balligand JL, Ungureanu D, Kelly RA, et al (1993) Abnormal contractile function due to induction of nitric oxide synthesis in rat cardiac myocytes follows exposure to activated macrophage-conditioned medium. J Clin Invest 91: 2314–2319

    Article  PubMed  CAS  Google Scholar 

  29. Brady AJB, Poole-Wilson PA, Harding SE, et al (1992) Nitric oxide production within cardiac myocytes reduces their contractility in endotoxemia. Am J Physiol 263 (Heart Circ Physiol 32): H1963-H1966

    PubMed  CAS  Google Scholar 

  30. Trautwein W, Trube G (1976) Negative inotropic effect of cyclic GMP in cardiac fiber fragments. Pflueger Arch 366: 293–295

    Article  CAS  Google Scholar 

  31. Petros A, Lamb G, Leone A, et al (1994) Effects of nitric oxide synthase inhibitor in humans with septic shock. Cardiovasc Res 28: 34–39

    Article  PubMed  CAS  Google Scholar 

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Authors
  1. M. Flesch
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  2. H. Kilter
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  3. M. Böhm
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Editor information

Editors and Affiliations

  1. Department of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, B-1070, Brussels, Belgium

    Jean-Louis Vincent (Clinical Director) (Clinical Director)

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© 1996 Springer-Verlag Berlin Heidelberg

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Flesch, M., Kilter, H., Böhm, M. (1996). Changes in Cardiac Signal Transduction in Septic Shock. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine. Yearbook of Intensive Care and Emergency Medicine, vol 1996. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80053-5_5

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  • DOI: https://doi.org/10.1007/978-3-642-80053-5_5

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-60552-2

  • Online ISBN: 978-3-642-80053-5

  • eBook Packages: Springer Book Archive

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