Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation

[1]  P. Boekstegers,et al.  Peripheral oxygen availability within skeletal muscle in sepsis and septic shock: Comparison to limited infection and cardiogenic shock , 1991, Infection.

[2]  P. Suter,et al.  Delivery dependent oxygen consumption in patients with septic shock: Daily variations, relationship with outcome and the sick-euthyroid syndrome , 2005, Intensive Care Medicine.

[3]  P. Boekstegers,et al.  Tnf-α and IL-1α inhibit both pyruvate dehydrogenase activity and mitochondrial function in cardiomyocytes: Evidence for primary impairment of mitochondrial function , 1997, Molecular and Cellular Biochemistry.

[4]  G. Van den Berghe,et al.  Metabolic, endocrine, and immune effects of stress hyperglycemia in a rabbit model of prolonged critical illness. , 2003, Endocrinology.

[5]  P. Venditti,et al.  Effect of thyroid state on rate and sites of H2O2 production in rat skeletal muscle mitochondria. , 2003, Archives of biochemistry and biophysics.

[6]  M. Astiz,et al.  Impaired mitochondrial function induced by serum from septic shock patients is attenuated by inhibition of nitric oxide synthase and poly(ADP-ribose) synthase* , 2003, Critical care medicine.

[7]  Marcos Intaglietta,et al.  Microvascular oxygen distribution in awake hamster window chamber model during hyperoxia. , 2003, American journal of physiology. Heart and circulatory physiology.

[8]  M. Singer,et al.  Mitochondrial Dysfunction in Sepsis. , 1999, Current infectious disease reports.

[9]  P. Seibel,et al.  Glucocorticoid and thyroid hormone receptors in mitochondria of animal cells. , 2003, International review of cytology.

[10]  Duchen,et al.  Decrease in VO2 in renal tubules from septic rats relates to clinical severity and nitric oxide , 2002 .

[11]  John Land,et al.  Association between mitochondrial dysfunction and severity and outcome of septic shock , 2002, The Lancet.

[12]  Jean-Charles Preiser,et al.  Microvascular blood flow is altered in patients with sepsis. , 2002, American journal of respiratory and critical care medicine.

[13]  M. Rigoulet,et al.  Thyroid Status Is a Key Regulator of Both Flux and Efficiency of Oxidative Phosphorylation in Rat Hepatocytes , 2002, Journal of bioenergetics and biomembranes.

[14]  R. Tompkins,et al.  Inducible nitric oxide synthase plays a role in LPS-induced hyperglycemia and insulin resistance. , 2002, American journal of physiology. Endocrinology and metabolism.

[15]  E. Ivers,et al.  Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock , 2001 .

[16]  M Schetz,et al.  Intensive insulin therapy in critically ill patients. , 2001, The New England journal of medicine.

[17]  J. Ligtenberg,et al.  Hormones in the critically ill patient: to intervene or not to intervene? , 2001, Intensive Care Medicine.

[18]  J. Mazat,et al.  Relationships between muscle mitochondrial metabolism and stress-induced corticosterone variations in rats , 2001, Pflügers Archiv.

[19]  K. Nair,et al.  T(3) increases mitochondrial ATP production in oxidative muscle despite increased expression of UCP2 and -3. , 2001, American journal of physiology. Endocrinology and metabolism.

[20]  J. C. Howie,et al.  Renal and respiratory failure in Scottish ICUs , 2001, Anaesthesia.

[21]  Rocco Barazzoni,et al.  Erratum: T3 increases mitochondrial ATP production in oxidative muscle despite increased expression of UCP2 and -3 (American Journal of Physiology - Endocrinology and Metabolism (E761-E769)) , 2001 .

[22]  R. Little,et al.  Insulin resistance and substrate utilization in human endotoxemia. , 2000, The Journal of clinical endocrinology and metabolism.

[23]  G. Brown,et al.  Reversal of nitric oxide-, peroxynitrite- and S-nitrosothiol-induced inhibition of mitochondrial respiration or complex I activity by light and thiols. , 2000, Biochimica et biophysica acta.

[24]  D. Annane,et al.  A 3-level prognostic classification in septic shock based on cortisol levels and cortisol response to corticotropin. , 2000, JAMA.

[25]  G. Van den Berghe,et al.  Increased mortality associated with growth hormone treatment in critically ill adults. , 2000, The New England journal of medicine.

[26]  John P. Johnson,et al.  A trial of thyroxine in acute renal failure. , 2000, Kidney international.

[27]  M. Singer,et al.  Mitochondrial dysfunction in sepsis , 2003, Current infectious disease reports.

[28]  C. King,et al.  Ileal mucosal oxygen consumption is decreased in endotoxemic rats but is restored toward normal by treatment with aminoguanidine. , 1999, Critical care medicine.

[29]  N R Webster,et al.  Increased mortality associated with growth hormone treatment in critically ill adults. , 1999, The New England journal of medicine.

[30]  C. Rivier,et al.  Nitric Oxide Stimulates ACTH Secretion and the Transcription of the Genes Encoding for NGFI-B, Corticotropin-Releasing Factor, Corticotropin-Releasing Factor Receptor Type 1, and Vasopressin in the Hypothalamus of the Intact Rat , 1999, The Journal of Neuroscience.

[31]  R. Hotchkiss,et al.  Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction. , 1999, Critical care medicine.

[32]  A. M. Cabanillas,et al.  Nitric oxide donors inhibit iodide transport and organification and induce morphological changes in cultured bovine thyroid cells. , 1998, Thyroid : official journal of the American Thyroid Association.

[33]  G. Van den Berghe,et al.  Clinical review 95: Acute and prolonged critical illness as different neuroendocrine paradigms. , 1998, The Journal of clinical endocrinology and metabolism.

[34]  P. Rothwell,et al.  Prediction of outcome in intensive care patients using endocrine parameters. , 1995, Critical care medicine.

[35]  C. Hinds,et al.  Elevation of systemic oxygen delivery in the treatment of critically ill patients. , 1994, The New England journal of medicine.

[36]  C. Rivier,et al.  In the rat, endogenous nitric oxide modulates the response of the hypothalamic-pituitary-adrenal axis to interleukin-1 beta, vasopressin, and oxytocin , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[37]  S. Matthaei,et al.  Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock , 1993, Critical care medicine.

[38]  K. M. Chen,et al.  Catecholamines: important factors in the increase of oxidative phosphorylation coupling in rat-liver mitochondria during the early phase of burn injury. , 1993, Burns : journal of the International Society for Burn Injuries.