Time-Dependent Changes in Donor Brain Death Related Processes

Schuurs, Theo A.; Morariu, Aurora M.; Ottens, Petra J.; Hart, Tony; Popma, Siccoc H; Leuvenink, Henri G. D.; Ploeg, Rutger J.

doi:10.1111/j.1600-6143.2006.01547.x

Cited by 73 publications

(73 citation statements)

References 41 publications

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“…The BD induction model is comprehensively detailed elsewhere (19,20). In short, after anesthesia, frontolateral trepanation was performed lateral of the bregma and a balloon was inserted.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Early Events in Kidney Donation: Progression of Endothelial Activation, Oxidative Stress and Tubular Injury After Brain Death

Morariu

Schuurs

Leuvenink

et al. 2008

American Journal of Transplantation

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Cerebral injury leading to brain death (BD) causes major physiologic derangements in potential organ donors, which may result in vascular-endothelial activation and affect posttransplant graft function. We investigated the kinetic of pro-coagulatory and proinflammatory endothelial activation and the subsequent oxidative stress and renal tubular injury, early after BD declaration. BD was induced by slowly inflating a balloon-catheter inserted in the extradural space over a period of 30 min. Rats (n = 30) were sacrificed 0.5, 1, 2 or 4 h after BD-induction and compared with sham-controls. This study demonstrates immediate pro-coagulatory and pro-inflammatory activation of vascular endothelium after BD in kidney donor rats, proportional with the duration of BD. E-and P-Selectins, Aa /Bb -fibrinogen mRNA were abruptly and progressively up-regulated from 0.5 h BD onwards; P-Selectin membrane protein expression was increased; fibrinogen was primarily visualized in the peritubular capillaries. Plasma von Willebrand factor was significantly higher after 2 h and 4 h BD. Urine heart-fatty-acid-binding-protein and Nacetyl-glucosaminidase, used as new specific and sensitive markers of proximal and distal tubular damage, were found significantly increased after 0.5 h, with a maximum at 4 h. Unexpectedly, oxidative stress was detectable only late, after the installation of tubular injury, suggesting only a secondary role for hypoxia in triggering these injuries.

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“…The BD induction model is comprehensively detailed elsewhere (19,20). In short, after anesthesia, frontolateral trepanation was performed lateral of the bregma and a balloon was inserted.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Early Events in Kidney Donation: Progression of Endothelial Activation, Oxidative Stress and Tubular Injury After Brain Death

Morariu

Schuurs

Leuvenink

et al. 2008

American Journal of Transplantation

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“…Furthermore, in the blood of braindead patients, increased levels of IL-8, IL-10, and interferon-beta have been observed. [18][19][20] Elevated activity of chemokines such as intercellular adhesion molecule 1, vascular cell adhesion molecule, Eselectin, P-selectin, and monocyte chemoattractant protein 1 have also been shown. 18 In addition, as stated above, brain death is accompanied by an exacerbated oxidative process.…”

Section: Diastolic Blood Pressurementioning

confidence: 99%

“…[18][19][20] Elevated activity of chemokines such as intercellular adhesion molecule 1, vascular cell adhesion molecule, Eselectin, P-selectin, and monocyte chemoattractant protein 1 have also been shown. 18 In addition, as stated above, brain death is accompanied by an exacerbated oxidative process. Through oxidative stress and a more extensive inflammatory process, brain death causes an increase in systemic and renal vascular resistance, thus leading to growth in diastolic blood pressure.…”

Section: Diastolic Blood Pressurementioning

confidence: 99%

Untitled

Kwiatkowska

Domański²,

Bober³

et al. 2017

Exp Clin Transplant

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“…This significant ischemic state is marked by elevated serum lactate levels (8)(9)(10). Appropriate donor management with hemodynamic stabilization after brain death toward normotensive levels limits organ dysfunction (8,11) and decreases the severity of the inflammatory response after brain death, which is demonstrated by a decrease in the number of CD8-positive cells in glomeruli and interstitium (9) (4), S100b (12,13), (14,15), complement activation and coagulation disorders (16 (12,13). The timeprofile of release suggests a role for S100b in delayed reparative processes.…”

Section: Induction Of Brain Death Leads To Hemodynamic Changesmentioning

confidence: 99%

“…In this respect it is worthwhile mentioning that an inverse correlation has been demonstrated between serum levels of IL-6 and kidney graft survival (31,32) (Figure 1). (5,11,33). The question remains whether this is due to a short half life of these cytokines.…”

Section: Induction Of Brain Death Leads To Hemodynamic Changesmentioning

confidence: 99%

Signal Transduction Pathways Involved in Brain Death-Induced Renal Injury

Bouma¹,

Ploeg

Schuurs

2009

American Journal of Transplantation

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Kidneys derived from brain death organ donors show an inferior survival when compared to kidneys derived from living donors. Brain death is known to induce organ injury by evoking an inflammatory response in the donor. Neuronal injury triggers an inflammatory response in the brain, leading to endothelial dysfunction and the release of cytokines in the circulation. Serum levels of interleukin-6, -8, -10, and monocyte chemoattractant protein-1 (MCP-1) are increased after brain death. Binding with cytokine-receptors in kidneys stimulates activation of nuclear factor-kappa B (NF-j B), selectins, adhesion molecules and production of chemokines leading to cellular influx. Mitogenactivated protein kinases (MAP-kinases) mediate inflammatory responses and together with NF-j B they seem to play an important role in brain death induced renal injury. Altering the activation state of MAPkinases could be a promising drug target for early intervention to reduce cerebral injury related donor kidney damage and improve outcome after transplantation.

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Time-Dependent Changes in Donor Brain Death Related Processes

Cited by 73 publications

References 41 publications

Early Events in Kidney Donation: Progression of Endothelial Activation, Oxidative Stress and Tubular Injury After Brain Death

Early Events in Kidney Donation: Progression of Endothelial Activation, Oxidative Stress and Tubular Injury After Brain Death

Untitled

Signal Transduction Pathways Involved in Brain Death-Induced Renal Injury

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