We sought to determine whether brain death-induced catecholamine release preconditions the heart, and if not, whether it precludes further protection by repetitive ischemia or isoflurane. Anesthetized rabbits underwent 30 min of coronary occlusion and 4 hours of reperfusion. The effect on infarct size of either no intervention (controls), ischemic preconditioning (IPC), or isoflurane inhalation (Iso), was evaluated with or without previous brain death (BD), induced by subdural balloon inflation. Plasma catecholamine levels were measured at several time points. Although it dramatically increase plasma catecholamine levels, brain death failed to reduce infarct size that averaged 0.49±0.34 without, versus 0.45±0.27 g with BD. IPC and Iso, alone as well as following brain death, significantly reduced infarct size, that averaged 0.11±0.04*, 0.21±0.15*, 0.10±0.09* and 0.22±0.10 g* in IPC, Iso, BD+IPC and BD+Iso groups, respectively (mean±SD, *p<0.05 vs controls). Brain death-induced catecholamines "storm" does not precondition the rabbit heart that however retains the ability to be protected by repetition of brief ischemia or isoflurane inhalation.