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Nitric Oxide as a Mediator in Gram-Positive Sepsis

  • J. Wilkinson
  • S. Sriskandan
  • J. Cohen
Part of the Update in Intensive Care and Emergency Medicine book series (UICM, volume 24)

Abstract

Sepsis and its sequelae are a cause of significant morbidity and mortality worldwide [1], due in part to a rise in the incidence of nosocomial infections as a consequence of the increased use of invasive procedures. Septic shock is now the commonest cause of death on intensive care units (ICU) in the US [2]. Traditionally, septic shock has been attributed to gram-negative infections, but it may be caused by gram-positive bacteria and other organisms. Gram-positive bacteria are increasingly being recognized as the cause of septic shock and sepsis syndromes [3]; in most series, they account for 40–50% of cases of bacteremia, and the mortality is at least as high as that seen complicating gram-negative infections.

Keywords

Nitric Oxide Septic Shock Necrotizing Fasciitis Adult Respiratory Distress Syndrome Toxic Shock Syndrome 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    The Working Group on Severe Streptococcal Infections (1993) Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. JAMA 269:390–391CrossRefGoogle Scholar
  2. 2.
    Parrillo JE (1990) Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Ann Intern Med 113:227–242PubMedGoogle Scholar
  3. 3.
    Shaunak S, Wendon J, Monteil M, Gordon AM (1988) Septic scarlet fever due to Streptococcus pyogenes cellulitis. Q J Med 69:921–925PubMedGoogle Scholar
  4. 4.
    Cohen J, Donnelly JP, Worsley AM, Catovsky D, Goldman JM, Galton DAG (1983) Septicaemia caused by viridans streptococci in neutropenic patients with leukaemia. Lancet 2:1452–1454PubMedCrossRefGoogle Scholar
  5. 5.
    Stevens DL, Tanner MH, Winship J, et al (1989) Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. N Engl J Med 321:1–7PubMedCrossRefGoogle Scholar
  6. 6.
    Hoge CW, Schwartz B, Talkington DF, Breiman RF, MacNeill EM, Englender SJ (1993) The changing epidemiology of invasive group A streptococcal infections and the emergence of streptococcal toxic shock-like syndrome. A retrospective population based study. JAMA 269:384–389PubMedCrossRefGoogle Scholar
  7. 7.
    Moncada S, Palmer RM, Higgs EA (1991) Nitric oxide: Physiology, pathophysiology, and pharmacology. Pharmacol Rev 43:109–142PubMedGoogle Scholar
  8. 8.
    Nathan C (1992) Nitric oxide as a secretory product of mammalian cells. FASEB J 6:3051–3064PubMedGoogle Scholar
  9. 9.
    Evans TJ, Carpenter A, Kinderman H, Cohen J (1993) Evidence of increased nitric oxide production in patients with the sepsis syndrome. Circ Shock 41:77–81PubMedGoogle Scholar
  10. 10.
    Finkel MS, Oddis CV, Jacob TD, Watkins SC, Hattler BG, Simmons RL (1992) Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 257:387–389PubMedCrossRefGoogle Scholar
  11. 11.
    Stevens DL (1992) Invasive group A streptococcus infections. Clin Infect Dis 14:2–13PubMedCrossRefGoogle Scholar
  12. 12.
    Bayston KF, Tomlinson M, Cohen J (1992) In-vitro stimulation of TNF-α from human whole blood by cell-free supernatants of gram-positive bacteria. Cytokine 4:397–402PubMedCrossRefGoogle Scholar
  13. 13.
    Rothstein JL, Schreiber H (1988) Synergy between tumor necrosis factor and bacterial products causes hemorrhagic necrosis and lethal shock in normal mice. Proc Natl Acad Sci USA 85:607–611PubMedCrossRefGoogle Scholar
  14. 14.
    Heremans H, Van Damme J, Dillen C, Dijkmans R, Billiau A (1990) Interferon gamma, a mediator of lethal lipoloysaccharide-induced Shwartzman-like shock reactions in mice. J Exp Med 171:1853–1869PubMedCrossRefGoogle Scholar
  15. 15.
    Evans TJ, Carpenter A, Silva AT, Cohen J (1992) Differential effects of monoclonal antibodies to tumor necrosis factor α and interferon gamma on induction of hepatic nitric oxide synthase in experimental gram-negative sepsis. Infect Immun 60:4133–4139PubMedGoogle Scholar
  16. 16.
    Marks JD, Marks CB, Luce JM, et al (1990) Plasma tumor necrosis factor in patients with septic shock. Mortality rate, incidence of adult respiratory distress syndrome, and effects of methyl prednisolone administration. Am Rev Respir Dis 141:94–97PubMedGoogle Scholar
  17. 17.
    Calandra T, Baumgartner JD, Grau GE, et al (1990) Prognostic values of tumor necrosis factor/cachectin, interleukin-1, interferon-alpha, and interferon-gamma in the serum of patients with septic shock. J Infect Dis 161:982–987PubMedCrossRefGoogle Scholar
  18. 18.
    Longchampt MO, Auguet M, Delaflotte S, Goulin-Schulz J, Chabrier PE, Braquet P (1992) Lipoteichoic acid: A new inducer of nitric oxide synthase. J Cardiovasc Pharmacol 20 (Suppl 12):S145-S147Google Scholar
  19. 19.
    Timmerman CP, Mattsson E, Martinez-Martinez L, et al (1993) Induction of release of tumor necrosis factor from human monocytes by staphylococci and staphylococcal peptidoglycans. Infect Immun 61:4167–4172PubMedGoogle Scholar
  20. 20.
    Zembrowicz A, Vane JR (1992) Induction of nitric oxide synthase activity by toxic shock syndrome toxin 1 in a macrophage-monocyte cell line. Proc Natl Acad Sci USA 89:2051–2055CrossRefGoogle Scholar
  21. 21.
    Cunha FQ, Moss DW, Leal LM, Moncada S, Liew FY (1993) Induction of macrophage parasiticidal activity by Staphylococcus aureus and exotoxins through the nitric oxide synthesis pathway. Immunology 78:563–567PubMedGoogle Scholar
  22. 22.
    Baud L, Cadranel J, Offenstadt G, Luquel L, Guidet B, Amstutz P (1990) Tumor necrosis factor and septic shock. Crit Care Med 18:349–350PubMedCrossRefGoogle Scholar
  23. 23.
    Schneider F, Lutun P, Runge I, Couchot A, Tempe JD (1992) Effects of soluble guanylyl cyclase inhibition by methylene blue on the loss of vascular responsiveness to norepinephrine in human beings with either gram-negative or gram-positive septic shock. Clin Intensive Care 3 (Suppl): 11 (Abst)Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1995

Authors and Affiliations

  • J. Wilkinson
  • S. Sriskandan
  • J. Cohen

There are no affiliations available

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