Abstract
Knowledge of the biochemical events linked to the development of necrosis in ischaemic heart muscle is relevant to the successful application of several new clinical techniques. Attempts to reper-fuse ischaemic tissue either by coronary angioplasty, thrombolytic therapy or vasodilator drugs, would be more likely to succeed, if the ultimate necrosis of myocardial tissue could be delayed or preferably prevented, allowing more time for the introduction of an intervention. Ischaemia of myocardial tissue must eventually result in tissue necrosis and the sequence of events during that process has been widely studied. Tissue survival is only possible if perfusion is re-established. A distinction has been made between the events during continuing ischaemia and the events occurring on reperfusion or reoxygenation. Phrases such as “reperfusion damage” or “the oxygen paradox” (Hearse et al., 1978) have been coined because some of the events on reperfusion or reoxygenation, such as enzyme release or calcium gain, are those associated with an exacerbation of cell damage. Nevertheless the hurdle of reoxygenation or reperfusion must be surmounted if the prevention of necrosis is to be a possible objective.
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© 1983 Plenum Press, New York
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Poole-Wilson, P.A. (1983). Mechanism of Cell Death in Myocardial Ischaemia. In: Dintenfass, L., Julian, D.G., Seaman, G.V.F. (eds) Heart Perfusion, Energetics, and Ischemia. NATO Advanced Science Institutes Series, vol 62. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0393-1_12
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DOI: https://doi.org/10.1007/978-1-4757-0393-1_12
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