Effects of Brain Death and Hemodynamic Status on Function and Immunologic Activation of the Potential Donor Liver in the Rat

Hoeven, Joost A. B. van der; Horst, Gert J. Ter; Molema, Grietje; Vos, Paul De; Girbes, Armand R.J.; Postema, Folkert; Freund, Reni L.; Wiersema, Janneke; Schilfgaarde, R. van; Ploeg, Rutger J.

doi:10.1097/00000658-200012000-00009

Cited by 133 publications

(95 citation statements)

References 25 publications

(21 reference statements)

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“…A hypotensive period after the catecholamine-induced peak has been described in most studies using a sudden onset model , Bittner et al 1995, Chen et al 1996, Herijgers et al 1996, van der Hoeven et al 2000. In our experiments, the peak in blood pressure occurred, followed by a plateau at levels above 100 mmHg ( Figure 1B).…”

Section: Discussionsupporting

confidence: 75%

The gradual onset brain death model: a relevant model to study organ donation and its consequences on the outcome after transplantation

et al. 2007

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SummaryOrgans used for transplantation are usually derived from heart-beating brain dead donors. However, brain death is known to have negative effects on donor organ quality, previously studied using a difficult to control sudden onset experimental model. We have now developed a reproducible gradual onset brain death model in rats without requiring inotropic support. Fisher inbred rats weighing 260-300 g were used. Brain death was induced by a gradual inflation of a subdurally placed balloon catheter. During induction and the period following brain death, the animals were mechanically ventilated and blood pressure was continuously monitored. The blood pressure registration showed a characteristic pattern during brain death induction, in which a decrease in blood pressure, a hypotensive period in which the Cushing response occurred, and a sharp peak were consistent findings. After brain death was induced, blood pressure was maintained at normotensive levels up to 4 h. After the experiments, neuropathological evaluation of the brain located haemorrhagic cerebral parenchyma, and immunocytochemistry of liver tissue revealed a significant influx of polymorph nuclear cells, as was previously observed as well. This improved model allows the study of brain death on donor organ quality without the use of inotropic support.

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Section: Discussionsupporting

confidence: 75%

The gradual onset brain death model: a relevant model to study organ donation and its consequences on the outcome after transplantation

et al. 2007

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“…CINC-3, a chemokine synonymous to rat macrophage inflammatory protein-2 (MIP-2), is strongly chemotactic for neutrophils and known to elicit a neutrophilic inflammatory response (30). These data explain the previous observation of increased neutrophilic infiltration in liver and kidneys within 6 h after brain death in the rat (17,26).…”

Section: Discussionmentioning

confidence: 55%

“…The donor BAL IL-8 concentration correlated with recipient graft function (7). Similar immune activation has been demonstrated in other organs with controlled animal experiments (17,26). However, cytokine responses in the lung have not been investigated in brain death models or in NPE.…”

Section: Introductionmentioning

confidence: 54%

“…Van der Hoeven et al optimized the arterial blood pressure of brain-dead rats using colloid infusion and noradrenaline. Donor optimization resulted in better kidney and liver function, but did not inhibit the inflammatory and immunological response in the liver, which increased progressively with time (26). In a similar study from the same group, maintaining donor normotension was found to delay progression of immunological activation in the kidneys (44).…”

Section: Discussionmentioning

confidence: 93%

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The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Avlonitis

Wigfield

Kirby

et al. 2005

American Journal of Transplantation

156

123

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Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by a -adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.

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“…In 1995, Terasaki et al 3 showed that graft survival for living unrelated donation is superior compared to deceased donation. This thought to be due to numerous pathophysiologic changes that occur in brain death that potentially contribute to DGF in the transplanted kidney 4 .…”

Section: Commentarymentioning

confidence: 99%

Targeted temperature management in deceased organ donors

Kadir

Al‐Khafaji

2016

F1000Res

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An evaluation of a recent study by Niemann CU, Feiner J, Swain S et al. The authors declare that they have no competing interests. Competing interests:The author(s) declared that no grants were involved in supporting this work. Grant information:© 2016 Kadir S and Al-Khafaji A. This is an open access article distributed under the terms of the Copyright:Creative Commons Attribution , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background There are about 16,000-17,000 renal transplants per year in the United States. Greater than 60% are deceased donor transplants. Up to 50% of these cases are complicated by delayed graft function (DGF), characterized by a requirement for dialysis in the recipient within 7 days after renal transplant. DGF is associated with an increased risk for an acute rejection episode. It is an independent risk factor for decreased graft survival and prolonged. Ischemiareperfusion injury during the transplantation process is also a major contributing factor to subsequent poor allograft function.

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Effects of Brain Death and Hemodynamic Status on Function and Immunologic Activation of the Potential Donor Liver in the Rat

Cited by 133 publications

References 25 publications

The gradual onset brain death model: a relevant model to study organ donation and its consequences on the outcome after transplantation

The gradual onset brain death model: a relevant model to study organ donation and its consequences on the outcome after transplantation

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Targeted temperature management in deceased organ donors

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