Abstract
When the heart is subjected to brief periods of sublethal ischemia separated by reperfusion it becomes resistant to a more prolonged lethal ischemic insult, a phenomenon which has been shown to protect it against infarction, reperfusion arrhythmias, contractile dysfunction and contracture.1-4 This endogenous protective mechanism has been termed ischemic preconditioning,1 and appears to occur in all animal species studied,2,5-7 including man.8,9 The protection produced by ischemic preconditioning is very potent but is short lived and decreases with time, lasting for an hour in most species. However a delayed or second window of protection (SWOP) has also been observed as a consequence of ischemic preconditioning; this protection occurs many hours after the sublethal preconditioning ischemia.10-14 The underlying mechanisms via which ischemic preconditioning protects the heart have been partly characterised in both animals and in the human, and appears to involve adenosine receptor activation, protein kinase C mediation and the possible opening of ATP-dependent-potassium (KATP) channels. If the exact mechanism of preconditioning in man could be determined, then it might be possible to develop preconditioning-like pharmacological therapies for patients at risk of certain cardiovascular disorders.
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Carr, C.S., Yellon, D.M. (1997). Preconditioning in Human Muscle and Myocytes. In: Mentzer, R.M., Kitakaze, M., Downey, J.M., Hori, M. (eds) Adenosine, Cardioprotection and Its Clinical Application. Developments in Cardiovascular Medicine, vol 194. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-8736-5_12
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DOI: https://doi.org/10.1007/978-1-4419-8736-5_12
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