THE PATHOGENESIS OF SEPTIC SHOCK

[21] Erickson, de Sauvage, Kikly, Et al., Decreased sensitivity to tumour-necrosis factor but normal T-cell development in TNF receptor-2-deficient mice, Nature, 372, pp. 560-563, (1994)

[22] Casey, Balk, Bone, Plasma cytokine and endotoxin levels correlate with survival in patients with the sepsis syndrome, Ann Intern Med, 119, pp. 771-778, (1993)

[23] Springer, Traffic signals for lymphocyte recirculation and leukocyte emigration: the multistep paradigm, Cell, 76, pp. 301-314, (1994)

[24] Moncada, Palmer, Higgs, Nitric oxide: physiology, pathophysiology and pharmacology, Pharm Rev, 43, pp. 109-142, (1991)

[25] Evans, Carpenter, Kinderman, Cohen, Evidence of increased nitric oxide production in patients with the sepsis syndrome, Circ Shock, 41, pp. 77-81, (1993)

[26] Evans, Carpenter, Silva, Cohen, Inhibition of nitric oxide synthase in experimental Gram-negative sepsis, Journal of Infectious Diseases, 169, pp. 343-349, (1994)

[27] Hollenberg, Cunnion, Lawrence, Kelly, Parillo, Tumor necrosis factor depresses myocardial cell function: results using an in vitro assay of myocyte performance, Clin Res, 37, (1989)

[28] Parrillo, Burch, Shehamer, Parker, Natanson, Schuette, A circulating myocardial depressant substance in humans with septic shock, J Clin Invest, 76, pp. 1539-1553, (1985)

[29] Ognibene, Cunnion, Mechanisms of myocardial depression in sepsis, Crit Care Med, 21, pp. 6-8, (1993)

[30] Vincent, Bakker, Marecaux, Schandene, Khan, Dupont, Administration of anti-TNF antibody improves left ventricular function in septic shock patients, Chest, 101, pp. 810-815, (1992)

[21] Erickson, de Sauvage, Kikly, Et al., Decreased sensitivity to tumour-necrosis factor but normal T-cell development in TNF receptor-2-deficient mice, Nature, 372, pp. 560-563, (1994)

[22] Casey, Balk, Bone, Plasma cytokine and endotoxin levels correlate with survival in patients with the sepsis syndrome, Ann Intern Med, 119, pp. 771-778, (1993)

[23] Springer, Traffic signals for lymphocyte recirculation and leukocyte emigration: the multistep paradigm, Cell, 76, pp. 301-314, (1994)

[24] Moncada, Palmer, Higgs, Nitric oxide: physiology, pathophysiology and pharmacology, Pharm Rev, 43, pp. 109-142, (1991)

[25] Evans, Carpenter, Kinderman, Cohen, Evidence of increased nitric oxide production in patients with the sepsis syndrome, Circ Shock, 41, pp. 77-81, (1993)

[26] Evans, Carpenter, Silva, Cohen, Inhibition of nitric oxide synthase in experimental Gram-negative sepsis, Journal of Infectious Diseases, 169, pp. 343-349, (1994)

[27] Hollenberg, Cunnion, Lawrence, Kelly, Parillo, Tumor necrosis factor depresses myocardial cell function: results using an in vitro assay of myocyte performance, Clin Res, 37, (1989)

[28] Parrillo, Burch, Shehamer, Parker, Natanson, Schuette, A circulating myocardial depressant substance in humans with septic shock, J Clin Invest, 76, pp. 1539-1553, (1985)

[29] Ognibene, Cunnion, Mechanisms of myocardial depression in sepsis, Crit Care Med, 21, pp. 6-8, (1993)

[30] Vincent, Bakker, Marecaux, Schandene, Khan, Dupont, Administration of anti-TNF antibody improves left ventricular function in septic shock patients, Chest, 101, pp. 810-815, (1992)