In 1986 Murry and co-workers introduced the term ‘Ischemic Preconditioning’ (Murry et al., 1986). In this classical paper the authors referred to ischemic preconditioning as an adaptation to ischemic stress induced by repetitive short periods of ischemia and reperfusion. The protective effect comprised a reduction of energy consumption and a delay of the onset of lethal cell injury during ischemia resulting in a limitation of infarct size (Lukas ,1998).
A potential and very desirable spin-off of research on ischaemic preconditioning may be the development of pharmacological interventions that could mimic or induce myocardial endogenous states and could be applied at the time of reperfusion. This development was not included as a potential clinical implication in the original report by Murry et al. When cell death secondary to ischaemia/reperfusion is seen as a consequence of active signalling processes that can be interfered with (David et al.,2011).