Abstract
Myocardial metabolism depends on a high level of ATP, which is essential for contraction and relaxation. Under aerobic conditions ADP generated is recycled to ATP mainly by oxidative phosphorylation. However, a small part of ADP is degraded to AMP, thus entering purine interconversion and catabolism. As a consequence purine nucleotides are broken down to adenosine, inosine and hypoxanthine. Since the myocyte membrane is permeable for nucleosides and bases (1), there is a continous loss of preformed purines. Especially during periods of ischemia accompanied by a depletion of myocardial ATP and CP high amounts of these degradation compounds can be detected in coronary venous blood (2, 3, 4)
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© 1986 Plenum Press, New York
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Schopf, G., Rumpold, H., Müller, M.M. (1986). Purine Salvage in Rat Heart Myoblasts. In: Nyhan, W.L., Thompson, L.F., Watts, R.W.E. (eds) Purine and Pyrimidine Metabolism in Man V. Advances in Experimental Medicine and Biology, vol 195B. Springer, New York, NY. https://doi.org/10.1007/978-1-4684-1248-2_79
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DOI: https://doi.org/10.1007/978-1-4684-1248-2_79
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