The current treatment for end stage heart failure is heart transplantation (HTx). The majority of donor hearts are procured from brain stem death (BSD) donors, with poor clinical outcomes associated with HTx using BSD donor hearts. BSD donor hearts have been shown to promote primary graft dysfunction (PGD) and hinder patient recovery. Little is known about the mechanisms leading to the poor HTx outcomes associated with BSD donor use. Although there is some evidence of a so-called catecholamine storm that is elicited by the trauma that occurs in BSD donors, some research suggests BSD may act as a preconditioning mimetic. However, to date, no studies have investigated the impact that BSD and the associated catecholamine storm has on cardioprotective signalling in HTx. Methods: Sixteen crossbreed merino sheep were paired according to weight and blood compatibility. Animals were allocated into 4 experimental groups, Sham or BSD groups, donor (D) and recipients subjected to cold static storage (CSS) for each (n=4). Animals were cannulated, given general anaesthesia and intubated, following which a burr hole was created with a 16 Fr Foley catheter to induce BSD via inflation of the Foley catheter. Sham donors had Foley catheters inserted but without inflation. Biopsies were taken for both Sham-D and BSD-D. Animals then underwent an orthotopic heart transplant, donor hearts were transplanted into recipient sheep, further biopsies were taken after 6hrs monitoring post separation from cardiopulmonary bypass for Sham-CSS and BSD-CSS groups. Expression of cardioprotective proteins in tissue samples were analysed via western blot analysis. Correlations between protein expression and previously published concentrations of cytokines and cardiac damage markers were assessed. [...]