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

Abstract

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.

Donor pretreatment with carbamylated erythropoietin in a brain death model reduces inflammation more effectively than erythropoietin while preserving renal function*

“…Induction of brain death showed a consistent and uniform pattern in blood pressure as described before (25) and took approximately 30 mins. All animals were kept at a mean arterial pressure of at least 80 mm Hg during the experiment.…”

“…Brain death was induced as described previously (25). Briefly, the procedure was performed as follows.…”

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

“…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.…”

Short-Term Effects of Hydroxyethylstarch Resuscitation on Systemic and Regional Hemodynamics and Metabolism in a Brain-Dead Canine Model

“…The systemic hemodynamic changes observed in brain-dead donors, as well as the extent of catecholamine release, depend on the rate of rise of intracranial pressure [20,[22][23][24]. We and others have been using a rapid and progressive increase in intracranial pressure in order to obtain a model that could reproduce the hemodynamic changes observed in marginal cadaveric donors [15][16][17][18].…”