By Barry L. Zaret MD, George A. Beller MD
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Extra resources for Clinical Nuclear Cardiology: State of the Art and Future Directions: Expert Consult: Online and Print, 4 Edition
Tracer retention needs to be long enough to allow imaging after stress. 201Tl has been a good example. If retention is too long, then the amount of redistribution will become insignificant. This seems to be the case with sestamibi and tetrofosmin. However, these tracers can give a good indication of regional wall thickening. Therefore, the best viability marker for these tracers may be the observation of disparity between regional perfusion and function. Redistribution is determined by membrane transport, not by blood flow.
The first is the ultimate conversion of the 6-carbon citrate to the 4-carbon oxaloacetate, which is then available for another “turn” of the TCA. This is linked to the second important product, carbon dioxide (CO2), which is produced through two decarboxylation steps, one mediated by isocitrate dehydrogenase and the other mediated by a-ketoglutarate dehydrogenase. This CO2 is released from the cell and ultimately leaves the body through the lungs. The third is the production of NADH2 by isocitrate dehydrogenase, a-ketoglutarate dehydrogenase, and malate dehydrogenase.
In Opie LH (ed): Heart Physiology: From Cell to Circulation, 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2004, pp 306-354. 50–52 These changes are due in part to alterations in the expression of the key transcriptional regulators, peroxisome proliferator activated receptor (PPAR)-a and peroxisome proliferator activated receptor-g coactivator (PGC)-1a. PPAR-a and PGC-1a interact in the nucleus to increase the transcription of a variety of genes that are primarily involved in mitochondrial biogenesis and fatty acid metabolism (Fig.