Abstract
Despite the upsurge of publications on ischemic preconditioning in recent years, the concept of preconditioning an organ with ischemia is not new. In 1986, Murry et al. demonstrated short periods of regional ischemia and reperfusion resulting in protection against necrosis to a later longer period of ischemia in the canine myocardium [1]. In reperfusion injury following a brief period of ischemia, tissues begin to adapt to anaerobic metabolism. Restoration of blood flow can lead to an oxygen supply that exceeds tissue requirements, the activation of macrophages, and the generation of reactive oxygen species [2]. This can ultimately result in endothelial injury and further release of pro-inflammatory cytokines [3]. Ischemic preconditioning occurs when a tissue undergoes brief periods of ischemia to later protect against longer ischemic events and reperfusion injury.
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