The Inflammatory Response to Brain Death

Barklin, Anne; Hvas, Christine Lodberg; Toennesen, Else

doi:10.1007/978-1-4614-4304-9_9

Cited by 7 publications

(11 citation statements)

References 86 publications

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“…Under the unstable metabolic conditions often seen in brain‐dead subjects 18 and the frequent requirement for high doses of catecholamine support, the information obtained might be very limited and non‐informative. The state of inflammation that accompanies brain death 19 might also influence the results. Furthermore, the public reaction to such an experiment would likely be mixed, and this might be detrimental to future progress in xenotransplantation.…”

Section: How Can This Obstacle Be Resolved?mentioning

confidence: 99%

The final obstacle to successful pre‐clinical xenotransplantation?

Yamamoto

Hara

Iwase

et al. 2020

Xenotransplantation

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Survival of non-human primates (NHPs) with life-supporting kidneys 1-4 or hearts 5 extends for many months. Attention has now turned towards phase transition to the first clinical trials. Ideally, the genetically engineered pig used as the source of the organs in the pre-clinical studies should be the same as that planned for the first clinical trials. Unfortunately, this will be difficult, and maybe impossible, because of differences in antibody binding to pig cells between humans and Old World NHPs. 6,7

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Section: How Can This Obstacle Be Resolved?mentioning

confidence: 99%

The final obstacle to successful pre‐clinical xenotransplantation?

Yamamoto

Hara

Iwase

et al. 2020

Xenotransplantation

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“…Inflammatory response [44] Observed [60] Observed [63] Observed [26] Few [64,66] Inotropic support [33] Applied [1,42] Applied [67] Not necessary [26,31] Not described Table 3. Reproducible clinical effects of brain death in the different experimental models.…”

Section: Discussionmentioning

confidence: 99%

“…A systemic inflammatory response is present in most patients at the diagnosis of BD [44]. The intense cellular and molecular activation that quickly follows the acute onset of BD involves acute transcriptional upregulation of inflammatory cytokines, both on a systemic and intraorgan level [16].…”

Section: Effects Of Brain Death On Liver Graft Undergoing Transplantamentioning

confidence: 99%

Experimental Brain Death Models in Liver Transplantation

Cornide‐Petronio¹,

Casillas-Ramírez²,

Jiménez‐Castro³

et al. 2018

Organ Donation and Transplantation - Current Status and Future Challenges

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Most organs for transplantation are currently procured from brain-dead donors; however, brain death is an important risk factor in liver transplantation. In addition, to counteract the shortage of liver grafts, transplant centers accept the use of sub-optimal livers, which may show higher risk of primary non-function or initial poor function. Very few literatures exist regarding liver transplantation using brain-dead donors, or about brain death and its effects on sub-optimal grafts in such surgical situation. This chapter aims to describe the pathophysiological changes occurring in liver grafts during brain death and focuses on the strengths and limitations of experimental models used to study the effect of brain death on optimal and sub-optimal (specially steatotic) liver grafts. Depending on the use of experimental models that simulate as much as possible the surgical conditions present in clinical practice, therapeutic strategies designed in animal models could be more successfully translated to the bedside.

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“…; Barklin et al . ). The management of brain‐dead potential donors aims to preserve the function of peripheral organs minimizing, therefore, the rate and intensity of acute rejection and graft dysfunction in the recipient (Barklin et al .…”

mentioning

confidence: 97%

“…Hemodynamic instability, microcirculatory dysfunction and inflammation triggered by brain death (BD) can compromise the viability of organs intended for transplantation (Barklin 2009;Chamorro et al 2009;Barklin et al 2013). The management of brain-dead potential donors aims to preserve the function of peripheral organs minimizing, therefore, the rate and intensity of acute rejection and graft dysfunction in the recipient (Barklin et al 2013). Acute brain injury can induce immunodeficiency thereby increasing morbidity and mortality after stroke, subarachnoid haemorrhage or trauma (Prass et al 2003;Liesz et al 2009).…”

mentioning

confidence: 99%

Evidence of bone marrow downregulation in brain‐dead rats

Menegat

Simas

Caliman

et al. 2017

Int J Experimental Path

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Experimental findings support the evidence of a persistent leucopenia triggered by brain death (BD). This study aimed to investigate leucocyte behaviour in bone marrow and blood after BD in rats. BD was induced using intracranial balloon catheter inflation. Sham-operated (SH) rats were trepanned only. Thereafter bone marrow cells were harvested every six hours from the femoral cavity and used for total and differential counts. They were analysed further by flow cytometry to characterize lymphocyte subsets, granulocyte adhesion molecules expression and apoptosis/necrosis [annexin V/propidium iodide (PI) protocol]. BD rats exhibited a reduction in bone marrow cells due to a reduction in lymphocytes (40%) and segmented cells (45%). Bone marrow lymphocyte subsets were similar in BD and SH rats (CD3, P = 0.1; CD4, P = 0.4; CD3/CD4, P = 0.4; CD5, P = 0.4, CD3/CD5, P = 0.2; CD8, P = 0.8). Expression of L-selectin and beta -integrins on granulocytes did not differ (CD11a, P = 0.9; CD11b/c, P = 0.7; CD62L, P = 0.1). There were no differences in the percentage of apoptosis and necrosis (Annexin V, P = 0.73; PI, P = 0.21; Annexin V/PI, P = 0.29). In conclusion, data presented suggest that the downregulation of the bone marrow is triggered by brain death itself, and it is not related to changes in lymphocyte subsets, granulocyte adhesion molecules expression or apoptosis and necrosis.

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The Inflammatory Response to Brain Death

Cited by 7 publications

References 86 publications

The final obstacle to successful pre‐clinical xenotransplantation?

The final obstacle to successful pre‐clinical xenotransplantation?

Experimental Brain Death Models in Liver Transplantation

Evidence of bone marrow downregulation in brain‐dead rats

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