Neuroendocrine Response and Shock

  • Riad N. YounesEmail author
  • Fernando C. Abrão


The concept of shock has evolved throughout the centuries, since the early descriptions of traumatic injury. Hippocrates (460–380 BC) recognized certain principles of wound care, such as elevating an injured limb; however, at that time the correlation between blood loss and death had not yet been identified. In the twentieth century, two physiologists, Cannon and Bayliss, developed studies in laboratory animals, postulating that systemic responses resulting from severe muscle injury were caused by a toxin that caused motor tonus loss, venous blood sequestration, and hypotension [1].


Growth Hormone Critical Illness Growth Hormone Administration Negative Nitrogen Balance Euthyroid Sick Syndrome 
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  1. 1.
    Cannon WB, Bayliss WM. Notes on muscle injury in relation to shock: special report of the Medical Research Commission. 1919;26:19.Google Scholar
  2. 2.
    Blalock A. Experimental shock, the cause of the low blood pressure produced by muscle injury. Arch Surg. 1930;22:959.CrossRefGoogle Scholar
  3. 3.
    Marchick MR, Kline JA, Jones AE. The significance of non-sustained hypotension in emergency department patients with sepsis. Intensive Care Med. 2009;35:1261–4.PubMedCrossRefGoogle Scholar
  4. 4.
    Demling R, LaLonde C, Saldinger P, Knox J. Multiple-organ dysfunction in the surgical patient: pathophysiology, prevention, and treatment. Curr Probl Surg. 1993;30:345.PubMedCrossRefGoogle Scholar
  5. 5.
    Hume DM, Egdahl RH. The importance of the brain in the endocrine response to injury. Ann Surg. 1959;150:697.PubMedCrossRefGoogle Scholar
  6. 6.
    Kehlet H. Modification of responses to surgery and anesthesia by neural blockade. In: Cousins MJ, Bridenbaugh PO, editors. Neural blockade in clinical anesthesia and management of pain. Philadelphia: J.B. Lippincott; 1987. p. 145.Google Scholar
  7. 7.
    Jeschke MG, Mlcak RP, Herndon DN. Morphologic changes of the liver after a severe thermal injury. Shock. 2007;28(2):172–7.PubMedCrossRefGoogle Scholar
  8. 8.
    Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med. 2008;34:17–60.PubMedCrossRefGoogle Scholar
  9. 9.
    Lavery GG, Glover P. The methabolic and nutritional response to critical illness. Curr Opin Crit Care. 2000;6:233–8.PubMedCrossRefGoogle Scholar
  10. 10.
    Arafah BM. Hypothalamic pituitary adrenal function during critical illness: limitations of current assessment methods. J Clin Endocrinol Metab. 2006;91:3725–45.PubMedCrossRefGoogle Scholar
  11. 11.
    Marik P. Critical illness-related corticosteroid insufficiency. Chest. 2009;135:181–93.PubMedCrossRefGoogle Scholar
  12. 12.
    Van den Berghe G, Wouters P, Bowers CY, et al. Growth hormone-releasing peptide-2 infusion synchronizes growth hormone, thyrotropin and prolactin release in prolonged critical illness. Eur J Endocrinol. 1999;140:17–22.PubMedCrossRefGoogle Scholar
  13. 13.
    Reichlin S. Neuroendocrine-immune inter-actions. N Engl J Med. 1993;329:1246–53.PubMedCrossRefGoogle Scholar
  14. 14.
    Goodall MC, Stone C, Haynes Jr BW. Urinary output of adrenaline and noradrenaline in severe thermal burns. Ann Surg. 1957;145:479–87.PubMedCrossRefGoogle Scholar
  15. 15.
    Wilmore DW, Aulick LH. Metabolic changes in burned patients. Surg Clin North Am. 1978;58:1173–87.PubMedGoogle Scholar
  16. 16.
    De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362:779–89.PubMedCrossRefGoogle Scholar
  17. 17.
    Reiss W, Pearson E, Artz CP. The metabolic response to burns. J Clin Invest. 1956;35:62–77.PubMedCrossRefGoogle Scholar
  18. 18.
    Newsome TW, Mason Jr AD, Pruitt Jr BA. Weight loss following thermal injury. Ann Surg. 1973;178:215–7.PubMedCrossRefGoogle Scholar
  19. 19.
    Hart DW, Wolf SE, Mlcak RP, et al. Persistence of muscle catabolism after severe burn. Surgery. 2000;128:312–9.PubMedCrossRefGoogle Scholar
  20. 20.
    Herndon D, Hart D, Wolf S, et al. Reversal of catabolism by beta-blockade after severe burns. N Engl J Med. 2001;345:1223–9.PubMedCrossRefGoogle Scholar
  21. 21.
    Gore DC, Wolfe RR. Hemodynamic and metabolic effects of selective beta1 adrenergic blockade during sepsis. Surgery. 2006;139:686–94.PubMedCrossRefGoogle Scholar
  22. 22.
    Baron PW, Barrow RE, Pierre EJ, et al. Prolonged use of propranolol safely decreases cardiac work in burned children. J Burn Care Rehabil. 1997;18:223–7.PubMedCrossRefGoogle Scholar
  23. 23.
    Panina-Bordignon P, Mazzeo D, Lucia PD, et al. Beta2-agonists prevent Th1 development by selective inhibition of interleukin-12. J Clin Invest. 1997;100:1513–9.PubMedCrossRefGoogle Scholar
  24. 24.
    Hasko G, Szabo C, Nemeth ZH, et al. Stimulation of beta-adrenoreceptors inhibits endotoxin-induced IL-12 production in normal and IL-10 deficient mice. J Neuroimmunol. 1998;88:57–61.PubMedCrossRefGoogle Scholar
  25. 25.
    Sanders VM, Baker RA, Ramer-Quinn DS, et al. Differential expression of the beta2- adrenergic receptor by TH1 and Th2 clones: implications for cytokine production and B cell help. J Immunol. 1997;158:4200–10.PubMedGoogle Scholar
  26. 26.
    Borger P, Hoekstra Y, Esselink MT, et al. Beta-adrenoceptor-mediated inhibition of IFN-gamma, IL-3, and GM-CSF mRNA accumulation in activated human T lymphocytes is solely mediated by the beta2-adrenoceptor subtype. Am J Respir Cell Mol Biol. 1998;19:400–7.PubMedCrossRefGoogle Scholar
  27. 27.
    Hasko G, Elenkov IJ, Kvetan V, et al. Differential effect of selective block of alpha 2-adrenoreceptors on plasma levels of tumor necrosisfactor – alpha, interleukin – 6 and corticosterone induced by bacterial lipopoly-saccharide in mice. J Endocrinol. 1995;144:457–62.PubMedCrossRefGoogle Scholar
  28. 28.
    Kovacs KJ, Elenkov IJ. Differential dependence of ACTH secretion induced by various cytokines on the integrity of the paraventricular nucleus. J Neuroendocrinol. 1995;7:15–23.PubMedCrossRefGoogle Scholar
  29. 29.
    Woiciechowsky CK, Asadullah K, Nestler D, et al. Sympathetic activation triggers systemic interleukin-10 release in immunodepression induced by brain injury. Nat Med. 1998;4:808–13.PubMedCrossRefGoogle Scholar
  30. 30.
    Fleshner M, Goehler LE, Schwartz BA, et al. Thermogenic and ­corticosterone responses to intravenous cytokines are attenuated by sub diaphragmatic vagotomy. J Neuroimmunol. 1998;86:134–41.PubMedCrossRefGoogle Scholar
  31. 31.
    Maier SF, Goehler LE, Fleshner M, et al. The role of the vagus nerve in cytokine-to-brain communication. Ann N Y Acad Sci. 1998;840:289–300.PubMedCrossRefGoogle Scholar
  32. 32.
    Watkins LR, Goehler LE, Relton JK, et al. Blockade of interleukin-1 induced hyperthermia by sub diaphragmatic vagotomy: ­evidence for vagal mediation of immune-brain communication. Neurosci Lett. 1995;183:27–31.PubMedCrossRefGoogle Scholar
  33. 33.
    Borovikova LV, Ivanova S, Zhang M, et al. Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. Nature. 2000;405:458–62.PubMedCrossRefGoogle Scholar
  34. 34.
    Guslandi M. Nicotine treatment for ulcerativecolitis. Br J Physiol Opt. 1998;274:L970–9.Google Scholar
  35. 35.
    Sandborn WJ. Transdermal nicotine for mildly to moderately active ulcerative colitis: a randomized, double-blind, placebo-controlled trial. Ann Intern Med. 1997;126:364–71.PubMedCrossRefGoogle Scholar
  36. 36.
    Sher ME. The influence of cigarette smoking on cytokine levels in patients with inflammatory bowel disease. Inflamm Bowel Dis. 1999;5:73–8.PubMedCrossRefGoogle Scholar
  37. 37.
    McEwen B. Protective and damaging effects of stress mediators. N Engl J Med. 1998;338:171–9.PubMedCrossRefGoogle Scholar
  38. 38.
    Seeman TE, Robbins RJ. Aging and hypothalamic-pituitary-adrenal response to challenge in humans. Endocr Rev. 1994;15:233–60.PubMedGoogle Scholar
  39. 39.
    Bessey PQ, Watters JM, Aoki TT, Wilmore DW. Combined hormonal infusion simulates the metabolic response to injury. Ann Surg. 1984;200:264.PubMedCrossRefGoogle Scholar
  40. 40.
    Wilmore DW. The metabolic management of the critically ill. New York: Plenum Medical; 1977.CrossRefGoogle Scholar
  41. 41.
    Annetta MG, Maviglia R, Proietti R, Antonelli M. Use of corticosteroids in critically ill septic patients: a review of mechanisms of adrenal insufficiency in sepsis and treatment. Curr Drug Targets. 2009;10:887–94.PubMedCrossRefGoogle Scholar
  42. 42.
    Marik P, Pastores SM, Annane D, Meduri GU, Sprung CL, Arlt W, et al. Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: consensus statements from an international task force by the American College of Critical Care Medicine. Crit Care Med. 2008;36:1937–49.PubMedCrossRefGoogle Scholar
  43. 43.
    Watt I, Ledingham IM. Mortality amongst multiple trauma patients admitted to an intensive therapy unit. Anaesthesia. 1984;39:973–81.PubMedCrossRefGoogle Scholar
  44. 44.
    Annane D, Sébille V, Troché G. A 3-level prognostic classification in septic shock based on cortisol levels and cortisol response to corticotropin. JAMA. 2000;283:1038–45. Short corticotropin test has prognostic value in predicting risk of death in sepsis.PubMedCrossRefGoogle Scholar
  45. 45.
    Galigniana MD, Piwien-Pilipuk G, Assreuy J. Inhibition of glucocorticoid receptor binding by nitric oxide. Mol Pharm. 1999;55:317–23.Google Scholar
  46. 46.
    Wohltmann CD, Spain DA, Carrillo EH. Does gender effect outcome in trauma patients? Crit Care Med. 1999;27:A176.CrossRefGoogle Scholar
  47. 47.
    Balteskard L, Unneberg K, Mjaaland M, et al. Treatment with growth hormone and insulin-like growth factor-1 in septicemia: effects on carbohydrate metabolism. Eur Surg Res. 1998;30:79–94.PubMedCrossRefGoogle Scholar
  48. 48.
    Chopra IJ. Clinical review 86. Euthyroid sick syndrome: is it a misnomer? J Clin Endocrinol Metab. 1997;82:329–834.PubMedCrossRefGoogle Scholar
  49. 49.
    Davies PH, Sheppard MC, Franklyn JA. Inflammatory cytokines and type I 5’-deiodinase expression in phi1 rat liver cells. Mol Cell Endocrinol. 1997;129:191–8.PubMedCrossRefGoogle Scholar
  50. 50.
    Brent GA, Hershman JM. Thyroxine therapy in patients with severe nonthyroidal illnesses and low serum thyroxine concentration. J Clin Endocrinol Metab. 1986;63:1–8.PubMedCrossRefGoogle Scholar
  51. 51.
    Aygen B, Inan M, Doganay M, Kelestimur F. Adrenal functions in patients with sepsis. Exp Clin Endocrinol Diabetes. 1997;105:182–6.PubMedCrossRefGoogle Scholar
  52. 52.
    Bornstein SR, Licinio J, Tauchnitz R, et al. Plasma leptin levels are increased in survivors of acute sepsis: associated loss of diurnal rhythm in cortisol and leptin secretion. J Clin Endocrinol Metab. 1998;83:280–3.PubMedCrossRefGoogle Scholar
  53. 53.
    Carlson GL, Saeed M, Little RA, Irving MH. Serum leptin concentrations and their relation to metabolic abnormalities in human sepsis. Am J Physiol. 1999;276:E658–62.PubMedGoogle Scholar
  54. 54.
    Van den Berghe G, Wouters P, Carlsson L, et al. Leptin levels in protracted critical illness; effects of growth hormone-secretagogues and thyrotropin-releassing hormone. J Clin Endocrinol Metab. 1998;83:3062–70.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag London 2013

Authors and Affiliations

  1. 1.Department of Surgery, Faculty of MedicineUniversity of Sao Paulo, Hospital Sao JoseSão PauloBrazil

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