Variation in the Levels of Inflammatory Cytokines Depending on Ischemic Time: Effects on Respiratory Variables

Durán, J. Arranz; González, Antonio; García, D. Domínguez; Falcón, R. Calvo; Pereda, Pablo Sanz; Alvarez, Susana; Cobaleda, I. García; Jaime, Armando Aguirre; González, Iván; Bosque, A. Varona; Gómez, Manuel Ángel Barrera; Lugo, A. Soriano Benitez de

doi:10.1016/j.transproceed.2009.01.045

Cited by 8 publications

(5 citation statements)

References 6 publications

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“…The duration and type (warm or cold) of ischaemic time may also directly influence cytokine production. A correlation was recently identified between cold ischaemia time and levels of IL-1 and IL-8 in human liver transplants [186]. Warm ischaemia time correlated with IL-6 and IL-10 in the same study.…”

Section: Stage Three Of Potential Organ Injury: Ischaemia Reperfussupporting

confidence: 61%

“…Warm ischaemia time correlated with IL-6 and IL-10 in the same study. Significantly, the authors found that the excess cytokines generated by hepatic graft warm ischaemia time resulted in systemic adverse effects, most notably increased intraoperative pulmonary shunt [186]. Another study found that, while cold ischaemic time per se did not adversely affect liver function, the associated graft-generated IL-8 did correlate with PGD [187].…”

Section: Stage Three Of Potential Organ Injury: Ischaemia Reperfusmentioning

confidence: 99%

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Inflammatory Signalling Associated with Brain Dead Organ Donation: From Brain Injury to Brain Stem Death and Posttransplant Ischaemia Reperfusion Injury

Watts

Thom

Fraser

2013

Journal of Transplantation

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Brain death is associated with dramatic and serious pathophysiologic changes that adversely affect both the quantity and quality of organs available for transplant. To fully optimise the donor pool necessitates a more complete understanding of the underlying pathophysiology of organ dysfunction associated with transplantation. These injurious processes are initially triggered by catastrophic brain injury and are further enhanced during both brain death and graft transplantation. The activated inflammatory systems then contribute to graft dysfunction in the recipient. Inflammatory mediators drive this process in concert with the innate and adaptive immune systems. Activation of deleterious immunological pathways in organ grafts occurs, priming them for further inflammation after engraftment. Finally, posttransplantation ischaemia reperfusion injury leads to further generation of inflammatory mediators and consequent activation of the recipient's immune system. Ongoing research has identified key mediators that contribute to the inflammatory milieu inherent in brain dead organ donation. This has seen the development of novel therapies that directly target the inflammatory cascade.

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Section: Stage Three Of Potential Organ Injury: Ischaemia Reperfussupporting

confidence: 61%

Section: Stage Three Of Potential Organ Injury: Ischaemia Reperfusmentioning

confidence: 99%

Inflammatory Signalling Associated with Brain Dead Organ Donation: From Brain Injury to Brain Stem Death and Posttransplant Ischaemia Reperfusion Injury

Watts

Thom

Fraser

2013

Journal of Transplantation

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“…A correlation was recently identified between cold ischaemia time and levels of IL-1 and IL-8 in human liver transplants. [223] Warm ischaemia time correlated with IL-6 and IL-10 in the same study.…”

Section: Contribution Of Preservation Strategies To Cytokine Expressionsupporting

confidence: 54%

“…[223] Another study found that, while cold ischaemic time per se did not adversely affect liver function, the associated graft generated IL-8 did correlate with PGD. [224] Weiss et al, in a study of transplanted human livers, showed that IL-4 was increased in BD donors prior to explantation, but cold ischaemia and reperfusion did not result in further increases in the cytokine.…”

Section: Contribution Of Preservation Strategies To Cytokine Expressionmentioning

confidence: 98%

The implications of brain death in donor lung injury: investigation and blockade of the endothelin axis

Watts¹

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“…Warm ischemia time also correlated with IL-6 and IL-10 in the same study. [54] Successful preservation strategies are key to minimize ischemic damage and the effect of reperfusion with associated increased immunogenicity after organ implantation. The current accepted standard for most solid organs is static cold storage (SCS), where the solid organ is stored on ice after removal from the donor, and then removed from the ice box at the time of implantation.…”

Section: Inflammation Limiting Strategies To Preserve Procured Organsmentioning

confidence: 99%

Pathophysiological Changes and Systemic Inflammation in Brain Dead Organ Donors: Effect on Graft Quality

Bezeljak¹,

Večerić-Haler²

2021

Organ Donation and Transplantation

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Transplantation is the definitive treatment of end-stage organ disease. As the shortage of suitable organs poses its main limitation, the active management of potential organ donors becomes increasingly more important. The majority of solid organs are still obtained from donors after confirmed brain death. Brain death is the complete and irreversible cessation of all brain functions, and triggers a variety of severe pathophysiological changes in cardiovascular, hormonal and metabolic status that can result in organ damage. Moreover, brain death is associated with massive inflammatory response with a cytokine storm and complement activation that increases graft immunogenicity and adversely affects graft survival. Organs from brain-dead donors are more prone to graft dysfunction and rejection when compared to organs obtained from living donors. Brain death is thus believed to be an important risk factor influencing the quality of organs before procurement.

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Variation in the Levels of Inflammatory Cytokines Depending on Ischemic Time: Effects on Respiratory Variables

Cited by 8 publications

References 6 publications

Inflammatory Signalling Associated with Brain Dead Organ Donation: From Brain Injury to Brain Stem Death and Posttransplant Ischaemia Reperfusion Injury

Inflammatory Signalling Associated with Brain Dead Organ Donation: From Brain Injury to Brain Stem Death and Posttransplant Ischaemia Reperfusion Injury

The implications of brain death in donor lung injury: investigation and blockade of the endothelin axis

Pathophysiological Changes and Systemic Inflammation in Brain Dead Organ Donors: Effect on Graft Quality

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