Summary
Reperfusion of the ischemic heart after a certain period of time has been shown to produce cell injury. There is evidence to show that alterations in mitochondrial metabolism during ischemia results in the accumulation of H+ in the cell and this then leads to the activation of Na+-H+ exchanger, Na+-Ca2+ exchanger and development of intracellular Ca2+-overload upon reperfusion. Changes in mitochondrial metabolism during ischemia and a massive release of catecholamines and their oxidation during reperfusion produce oxyradicals and other oxidants in the myocardium. This oxidative stress causes the depression of sarcolemmal Na+-K+ ATPase and Ca2+-pump ATPase and these changes also contribute towards the occurrence of intracellular Ca2+-overload. Both oxidative stress and intracellular Ca2+-overload produce changes in the sarcoplasmic reticular Ca2+-cycling proteins as well as myofibrillar proteins and these defects then result in contractile dysfunction in the ischemic-reperfused hearts. Ischemic preconditioning and some pharmacological interventions, which attenuate the development of intracellular Ca2+-overload, have been demonstrated to reduce ischemia-reperfusion injury. Thus it appears that intracellular Ca2+-overload plays a critical role in the induction of myocardial cell damage and heart dysfunction due to ischemia-reperfusion.
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Temsah, R.M., Netticadan, T., Dhalla, N.S. (2003). Mechanisms of Cellular Alterations Due to Ischemia-Reperfusion Injury in the Heart. In: Dhalla, N.S., Takeda, N., Singh, M., Lukas, A. (eds) Myocardial Ischemia and Preconditioning. Progress in Experimental Cardiology, vol 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0355-2_11
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DOI: https://doi.org/10.1007/978-1-4615-0355-2_11
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