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The Inflammatory Response to Brain Death

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The Brain-Dead Organ Donor

Abstract

Brain death is associated with a systemic inflammatory response detected as increased pro-inflammatory cytokines in plasma and increased expression of pro-inflammatory cytokines, adhesion molecules, and major histocompatability complex (MHC) class I and II in organs suitable for transplantation.

At organ level, inflammatory mediators appear to be more pronounced in the heart, liver, and lung in brain-dead patients than in living donors. Increased levels of inflammatory mediators in the donor are associated with poor outcome after transplantation. However, if biopsies are drawn before cold ischemia, there are no differences in inflammatory markers between brain-dead and living donors.

Large and small animal models of brain death show an inflammatory response at organ level. However, there seems to be a discrepancy between results reported in large animal (porcine and canine) models and in rodent studies. One important observation is that brain death does not induce an inflammatory response in studies where hypotension was prevented, i.e. if the animals were fluid resuscitated. It still remains unknown whether inflammation is induced by brain death itself or by events before or after becoming brain dead.

Anti-inflammatory treatment and interventions aiming to reduce inflammation after brain death may improve the quality of organs from brain-dead donors. However, as long as the pathophysiological mechanisms behind the development of organ dysfunction associated with brain death remain to be clarified, no interventions aimed at improving outcome have yet been introduced.

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Correspondence to Anne Barklin M.D., Ph.D. .

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Barklin, A., Hvas, C.L., Toennesen, E. (2013). The Inflammatory Response to Brain Death. In: Novitzky, D., Cooper, D. (eds) The Brain-Dead Organ Donor. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-4304-9_9

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