Abstract
Brain stem death (BD) causes increased levels of catecholamines which may induce β-adrenoceptor desensitisation and mitochondrial dysfunction. Combined, this contributes to donor heart dysfunction (DHD) and post-transplant graft failure. We sought to examine peri-transplant catecholamine sensitivity, cardiac contractility and mitochondrial function post-BD and transplantation (Tx) in a clinically relevant ovine model.
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