Abstract
The beating warm-blooded heart cannot tolerate ischemia and a reduction of oxygen delivery for more than a short time — one minute at most — without serious impairments of its function. From the point of view of the needs of energy of the muscle, this is not so much because the myocardial energy reserves (i.e., glycogen) may become exhausted, but rather because the rate of glycogenolysis is not high enough in mammalian heart muscle to compensate for this deficiency, in face of a continued utilization of high energy phosphate (HEP) and of low efficacy of the glycolysis, by an adequate synthesis of adenosine triphosphate (ATP) in the mitochondria. As well known, the majority (>90%) of myocardial ATP is produced aerobically by oxidative phosphorylation in the normal heart [1].
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Krause, EG., Pfeiffer, D., Wollenberger, U., Wollert, HG. (1993). Lactate monitoring during and after cardiopulmonary bypass: an approach implicating a perioperative measure for cardiac energy metabolism. In: Piper, H.M., Preusse, C.J. (eds) Ischemia-reperfusion in cardiac surgery. Developments in Cardiovascular Medicine, vol 142. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1713-5_14
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DOI: https://doi.org/10.1007/978-94-011-1713-5_14
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