Organ-specific regulation of pro-inflammatory molecules in heart, lung, and kidney following brain death

Skrabal, Christian; Thompson, Larry O.; Potapov, E.; Southard, Robert E.; Joyce, David L.; Youker, Keith A.; Noon, George P.; Loebe, Matthias

doi:10.1016/j.jss.2004.07.245

Cited by 84 publications

(29 citation statements)

References 33 publications

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“…The endotoxin, the activation of the complement, the cytokines, the arachidonic acid's metabolites, liposomal enzymes and kinines, histamine, the nitric oxide or the mediators derived from the endothelium, are the aggressive participants in the decompensation of the patient's clinical status. The complications arise together with micro-embolisms, pulmonary artery hypertension and the alteration of the respiratory functions [41][42][43][44][45][46][47][48]. Neutrophils stimulation through different biochemical mechanisms produces high quantities of hydrogen peroxide [49][50][51].…”

Section: Biochemical Aspects Of Free Radicals and The Actions Of Oxidmentioning

confidence: 99%

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Bedreag¹,

Rogobete

Sărăndan³

et al. 2015

Anaesthesiol Intensive Ther

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Multiple trauma patients require extremely good management and thus, the trauma team needs to be prepared and to be up to date with the new standards of intensive therapy. Oxidative stress and free radicals represent an extremely aggressive factor to cells, having a direct consequence upon the severity of lung inflammation. Pulmonary tissue is damaged by oxidative stress, leading to biosynthesis of mediators that exacerbate inflammation modulators. The subsequent inflammation spreads throughout the body, leading most of the time to multiple organ dysfunction and death. In this paper, we briefly present an update of biochemical effects of oxidative stress and free radical damage to the pulmonary tissue in patients in critical condition in the intensive care unit. Also, we would like to present a series of active substances that substantially reduce the aggressiveness of free radicals, increasing the chances of survival.

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Section: Biochemical Aspects Of Free Radicals and The Actions Of Oxidmentioning

confidence: 99%

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Bedreag¹,

Rogobete

Sărăndan³

et al. 2015

Anaesthesiol Intensive Ther

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“…This result is supported as the livers from a living donor have superior post-transplant survival rate compared with those from BD donors (22,23). This process was associated with the increased immune activation, including the increased release and expression of pro-inflammatory as well as anti-inflammatory cytokines (4,8).…”

Section: Discussionmentioning

confidence: 82%

“…Organ transplantation is often the only treatment option at end-stage organ diseases (2,4). Evidences have shown that BD causes inflammatory changes in the donors (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, a systemic inflammatory response in BD donors occurs, causing further damages to the organs, e.g. the increased inflammatory cytokines such as tumour necrosis factor alpha (TNF-α), Interleukin 1 beta (IL1B), Interleukin 6 (IL6), Interleukin 10 (IL10) and macrophage inflammatory protein 1-alpha (MIP-1α) in donor organs (4,9). In this context, the increased cold ischemia time, unspecific inflammatory events, additional recipient, and donor-related risk factors are crucial (10).…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of Gene Expression Pattern of IL1B and IL10 Cytokines Following Vitamin C Administration among Brain-Dead Liver Donors

Sisakht

Khosravi

Milani

et al. 2016

Iran Red Crescent Med J

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Background: Inflammatory events following brain death (BD) decrease the quality of donor organs which can affect the outcome of the transplantation. It experimentally and clinically is verified that the level of inflammatory cytokines is increased in the BD of the donor results. In experiments, the in vitro use of vitamin C can successfully decrease the levels of inflammatory cytokines. Objectives: The aim of this study was to investigate the influence of vitamin C administration on the inflammatory status of the graft in BD liver donors. Methods: This study was conducted at Nemazee Hospital's transplant center (Shiraz, Iran). In this interventional study, the BD liver donors (n = 40) were randomly divided into two groups. The control group received only the routine intensive care unit (ICU) considerations, and the intervention group was treated with Vitamin C before harvesting organ (100 mg/kg, initially followed by 100 mg/kg/6h until organ removal). Blood samples were taken from BD patients in the intervention and control groups 3 times: 6 hours before operation, immediately after laparotomy, and immediately prior to clamping the aorta to assess the gene expression ratio of Interleukin 1 beta (IL1B) and Interleukin 10 (IL10) cytokines using real time polymerase chain reaction (PCR) (n = 40). Soluble serum cytokines were measured by enzyme-linked immunosorbent assay (ELISA) (n = 24). Results: No significant differences were observed in mRNA expression ratio of IL1B and IL10 between two groups. Despite an acceptable decrease in serum concentration of the inflammatory markers IL1B and IL10 at time point 2 minus time point 1 (T2-1), no significant differences were observed in vitamin C-treated BD donors compared with the control donors. There was a significant difference among aspartate aminotransferase (AST) and alanine aminotransferase (ALT) changes on the 3rd to 1st days after operation between the control and intervention recipients (P < 0.05). Conclusions:The present study suggests a beneficial effect of vitamin C adsministration on post-transplant function of the liver from BD liver donors.

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“…Interpretation of some conflicting animal data regarding the reversibility of brain-death-related donor organ injury [28][29][30][31][32][33][34][35], has been limited by differences in models tested and because the mechanisms contributing to cardiopulmonary dysfunction following transplantation of brain-dead donor organs are not well defined. Despite common agreement that the inflammatory response to brain death is a crucial factor to overcome in order to improve subsequent graft function, the important early signalling of the pro-inflammatory mediator, p38 MAPK in brain-dead donor thoracic organs has not been fully elucidated.…”

Section: Donor Brain Death Is a Major Determinant Of Recipient Outcommentioning

confidence: 99%

p38 Mitogen-Activated Protein Kinase Inhibition Reduces Inflammatory Cytokines in a Brain-Dead Transplant Donor Animal Model

Oto

Calderone

Li³

et al. 2009

Heart, Lung and Circulation

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Organ-specific regulation of pro-inflammatory molecules in heart, lung, and kidney following brain death

Cited by 84 publications

References 33 publications

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Evaluation of Gene Expression Pattern of IL1B and IL10 Cytokines Following Vitamin C Administration among Brain-Dead Liver Donors

p38 Mitogen-Activated Protein Kinase Inhibition Reduces Inflammatory Cytokines in a Brain-Dead Transplant Donor Animal Model

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