Human Brain-Dead Donors and 31P MRS Studies on Feline Myocardial Energy Metabolism

In clinical heart transplantation, the heart of a brain dead donor is used. The quality of the donor heart is one of the key factors for a succesful transplantation. A hemodynamically unstable brain dead donor is often rejected because survival of the recipient is reduced.1–3 The precise mechanisms of brain death-related hemodynamic instability remain unknown. One of the reported contributing factors is myocardial injury resulting from the acutely increased discharge of endogenous catecholamines during the onset of brain death.4,5 This injury has been supposed to change aerobic to anaerobic energy metabolism, causing depletion of myocardial high-energy phosphates and contractile dysfunction.6–8 Energy depletion appeared to be even more pronounced when high dosages of inotropic agents were used to treat contractile dysfunction of the canine donor heart.9 Notwithstanding these results, the presence of anaerobic metabolism is disputed by others.10-13