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Metabolic Support for the Heart During Ischemia and Reperfusion: Role of Amino Acids

This chapter appears in the following book:

Ischemia-Reperfusion Injury in Cardiac Surgery

Edited by: Friedhelm Beyersdorf
ISBN: 1-58706-002-7
» Get more information about this book at landesbioscience.com «

Chapter authors:
Heinrich Taegtmeyer and Torsten Doenst

In reviewing amino acid metabolism of the heart during ischemia and reperfusion it is important to address a few principles of energy substrate metabolism first. The healthy human heart has a very high rate of energy turnover. Like all living cells, cardiac myocytes need the energy captured in ATP to power their essential functions. The bulk of it is derived from oxidative phosphorylation of ADP, which, in turn, is fueled by oxidation of substrates such as fatty acids, glucose, glycogen, lactate, and certain amino acids. The normal human heart, which weighs about 300 g, consumes about 5 kg of ATP in the course of 24 hours, i.e., 17 times its own weight!1 Under normal conditions most of the energy for contraction is derived from the oxidation of long-chain fatty acids,2 but inotropic stimulation results in the preferential oxidation of glycogen.3 The heart oxidizes amino acids only when their plasma concentrations are very high.4

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