1995
DOI: 10.1016/0026-0495(95)90198-1
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Blood levels of cytokines in brain-dead patients: Relationship with circulating hormones and acute-phase reactants

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Cited by 152 publications
(97 citation statements)
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“…Plasma HMGB1 levels were slightly elevated in organ donors already before graft procurement, reflecting a systemic proinflammatory response induced by brain death. [28][29][30] Furthermore, surgical manipulation of the liver during procurement activates Kupffer cells, leading to hepatic expression of proinflammatory mediators. 30,31 Indeed, weak hepatocyte HMGB1 staining was already evident in biopsies taken immediately before graft perfusion during procurement.…”
Section: Discussionmentioning
confidence: 99%
“…Plasma HMGB1 levels were slightly elevated in organ donors already before graft procurement, reflecting a systemic proinflammatory response induced by brain death. [28][29][30] Furthermore, surgical manipulation of the liver during procurement activates Kupffer cells, leading to hepatic expression of proinflammatory mediators. 30,31 Indeed, weak hepatocyte HMGB1 staining was already evident in biopsies taken immediately before graft perfusion during procurement.…”
Section: Discussionmentioning
confidence: 99%
“…[47][48][49][50] Increased expression of IL-6 and TNF-a has been related to malfunction of donor hearts and prediction of right ventricular failure after human heart transplantation. 51,52 In kidney transplantation, both short-and long-term results of unrelated living transplants are superior to even well-matched cadaveric transplants, [53][54][55] and increased cytokine levels in the blood and kidney of brain-dead donors compared with living donors reflect this difference in outcome between living and cadaveric donation.…”
Section: Inflammatory and Immunological Aspects Of Brain Deathmentioning
confidence: 99%
“…Although increased serum IL-6 levels were found in children with acute respiratory infections and in brain-dead patients, TNF-a and IL-1 concentrations were generally normal. 18,19 Boelen et al 36 studied the levels of interferon-g, IL-8 and IL-10 in ESS patients and found no evidence that they had a pathogenic role.…”
Section: Discussionmentioning
confidence: 99%
“…[13][14][15][16] Moreover, serum IL-6 levels were negatively correlated with serum FT 3 in ESS. [17][18][19][20][21][22][23] It is generally agreed that ESS is associated with increased cytokine production, but the degree of cytokine involvement and their specific roles in the pathogenesis of ESS remain to be elucidated.…”
mentioning
confidence: 99%