Cessation of blood flow after cardiac arrest is characterised by rapid development of profound tissue ischaemia in proportion to the metabolic needs of individual tissue beds [1] . Remarkably, very little cell injury is demonstrable during the interval of ischaemia when there is no blood flow. Injury, however, becomes evident upon reperfusion subsequent to the reintroduction of oxygen, generation of reactive oxygen species (ROS), and activation of a myriad of pathogenic pathways [2] . This

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... menon has been termed "reperfusion injury" and is now recognised as a major player of ischaemic injury. After ischaemia and reperfusion, a more protracted (post-ischaemic) phase begins, which manifests by varying degrees of cell dysfunction and cell death, as a result of apoptosis and cell necrosis. These processes have been well characterised in various cell systems and models of acute ischaemic injury, with the exclusion of cardiac arrest models. Yet, growing evidence points to a major role in the cardiac arrest setting, probably determining initial capability for re-establishing spontaneous circulation and subsequent capability for restoring organ function. Although cardiac arrest and resuscitation set the conditions for all tissues to suffer ischaemia and reperfusion injury, the most susceptible ones are also the most vital; namely, the heart and brain. There is a very narrow time-windows within which no flow or partial flow can be tolerated before irreversible injury develops. Current resuscitation protocols provide for interventions aimed at reversing the precipitating cause of cardiac arrest (i.e., terminating ventricular fibrillation, or correcting severe hypoxaemia) and artificially promoting blood flow across the coronary and cerebral circuits. However, no specific interventions are currently available that could target pathogenic pathways responsible for ischaemic and reperfusion injury. Yet, there is substantial interest and various research laboratories have begun to examine pharmacological interventions aimed at cell protection. In this chapter, we address primarily the myocardial effects of ischaemia and reperfusion, with emphasis on its functional consequences, mechanisms, and potential therapeutic implications.