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Artículos de revistas sobre el tema "Heart Metabolism"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 11 de febrero de 2022

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1

Belke, Darrell D., Terje S. Larsen, Gary D. Lopaschuk, and David L. Severson. "Glucose and fatty acid metabolism in the isolated working mouse heart." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 4 (October 1, 1999): R1210—R1217. http://dx.doi.org/10.1152/ajpregu.1999.277.4.r1210.

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Although isolated perfused mouse heart models have been developed to study mechanical function, energy substrate metabolism has not been examined despite the expectation that the metabolic rate for a heart from a small mammal should be increased. Consequently, glucose utilization (glycolysis, oxidation) and fatty acid oxidation were measured in isolated working mouse hearts perfused with radiolabeled substrates, 11 mM glucose, and either 0.4 or 1.2 mM palmitate. Heart rate, coronary flow, cardiac output, and cardiac power did not differ significantly between hearts perfused at 0.4 or 1.2 mM pa

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2

Giffin, Mitch, Gilbert Arthur, Patrick C. Choy, and Ricky Y. K. Man. "Lysophosphatidylcholine metabolism and cardiac arrhythmias." Canadian Journal of Physiology and Pharmacology 66, no. 2 (February 1, 1988): 185–89. http://dx.doi.org/10.1139/y88-032.

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The ability of exogenous lysophosphatidylcholine (LPC) to produce electrophysiological abnormalities in cardiac tissues and cardiac arrhythmias in isolated hearts has been well documented. In this study, the arrhythmogenic nature of LPC in the rat, rabbit, and guinea pig hearts was studied. The rat heart was found to be the most susceptible to LPC-induced arrhythmias, while the guinea pig heart was the least susceptible. Perfusion with labelled LPC revealed that the severity of arrhythmias correlates well with the amount of labelled LPC found in the microsomal membrane. The biochemical basis f

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3

Svensson, Sveneric, Rolf Svedjeholm, Rolf Ekroth, Italo Milocco, Folke Nilsson, Karl Göran Sabel, and Göran William-Olsson. "Trauma metabolism and the heart." Journal of Thoracic and Cardiovascular Surgery 99, no. 6 (June 1990): 1063–73. http://dx.doi.org/10.1016/s0022-5223(20)31463-x.

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4

FERRARA, R. "Myocardial metabolism: the diabetic heart." European Heart Journal Supplements 5 (January 2003): B15—B18. http://dx.doi.org/10.1016/s1520-765x(03)90036-8.

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5

GARLICK, P. B. "The Heart: Physiology and Metabolism." Cardiovascular Research 26, no. 1 (January 1, 1992): 85. http://dx.doi.org/10.1093/cvr/26.1.85.

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6

HAUGAARD, N., M. HESS, A. TORBATI, and O. TULP. "Energy metabolism in diabetic heart." Journal of Molecular and Cellular Cardiology 18 (1986): 32. http://dx.doi.org/10.1016/s0022-2828(86)80127-4.

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7

KAKO, K., and M. KATO. "Phospholipid metabolism in heart membranes." Journal of Molecular and Cellular Cardiology 18 (1986): 37. http://dx.doi.org/10.1016/s0022-2828(86)80140-7.

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8

Doenst, Torsten, Tien Dung Nguyen, and E. Dale Abel. "Cardiac Metabolism in Heart Failure." Circulation Research 113, no. 6 (August 30, 2013): 709–24. http://dx.doi.org/10.1161/circresaha.113.300376.

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9

Lesnefsky, Edward J., Qun Chen, and Charles L. Hoppel. "Mitochondrial Metabolism in Aging Heart." Circulation Research 118, no. 10 (May 13, 2016): 1593–611. http://dx.doi.org/10.1161/circresaha.116.307505.

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10

Donck, Kris. "Purine metabolism in the heart." Pharmacy World & Science 16, no. 2 (April 1994): 69–76. http://dx.doi.org/10.1007/bf01880658.

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11

Ventura-Clapier, Renée, Anne Garnier, and Vladimir Veksler. "Energy metabolism in heart failure." Journal of Physiology 555, no. 1 (February 15, 2004): 1–13. http://dx.doi.org/10.1113/jphysiol.2003.055095.

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12

Donck, Kris. "Purine metabolism in the heart." Pharmacy World & Science 16, no. 3 (June 1994): 166. http://dx.doi.org/10.1007/bf01877490.

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13

Da Dalt, L., L. Castiglioni, A. Baragetti, F. Pellegatta, M. Svecla, L. Sironi, N. Mitro, A. L. Catapano, and D. G. Norata. "PCSK9 deficiency and heart metabolism." Atherosclerosis 331 (August 2021): e15. http://dx.doi.org/10.1016/j.atherosclerosis.2021.06.049.

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14

Azuero, Rodrigo, Chittaranjan Debata, Marie Quinn, Kathleen McDonough, Jessica Thomson, and Duna Penn. "Dobutamine alters carnitine metabolism in the neonatal piglet heart." Canadian Journal of Physiology and Pharmacology 82, no. 7 (July 1, 2004): 493–501. http://dx.doi.org/10.1139/y04-048.

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The use of inotropic agents to support the neonatal heart after sepsis or hypoxia increases cardiac energy demand. Carnitine plays a vital role in energy, fuel metabolism. To test the hypothesis that inotropic agents affect carnitine metabolism, hearts from sow-fed piglets were isolated and perfused with an oxygenated buffer containing glucose and palmitate. Increasing dosages of dobutamine (DOB 2.5–15 µg/Kg body wt per min, 0.007–0.044 µmol/kg per min) or saline vehicle (SAL) were administered. Heart rate (HR), left ventricular systolic (LVSP) and end diastolic pressures (LVEDP) were measured

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15

Evans, R. D., M. J. Bennett, and D. Hauton. "Perfused heart studies to investigate lipid metabolism." Biochemical Society Transactions 28, no. 2 (February 1, 2000): 113–20. http://dx.doi.org/10.1042/bst0280113.

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The isolated perfused heart preparation is an invaluable model for investigating metabolism in a variety of physiological and pathological states. It avoids confounding systemic factors (e.g. endocrine, metabolic and work load changes) and permits simultaneous measurement of mechanical function. The ability to measure arteriovenous concentration differences across the myocardium and the coronary flow rate, together with the use of radiolabelled substrates, permits assessment of substrate assimilation and disposition of most potential energetic substrates. In the case of lipids, metabolism of n

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16

Mardy, Kai, Darrell D. Belke, and David L. Severson. "Chylomicron metabolism by the isolated perfused mouse heart." American Journal of Physiology-Endocrinology and Metabolism 281, no. 2 (August 1, 2001): E357—E364. http://dx.doi.org/10.1152/ajpendo.2001.281.2.e357.

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The catabolism of rat chylomicrons, labeled in their triacylglycerol (TG) component, was investigated using perfused working mouse hearts. Perfusion of mouse hearts with heparin increased lipoprotein lipase (LPL) activity in the perfusate. This heparin-releasable LPL pool remained constant over a variety of experimental conditions, including workload and fatty acid concentrations, making the mouse heart a suitable model to study chylomicron catabolism. Endothelium-bound LPL hydrolyzed radiolabeled 3H-labeled chylomicrons (0.4 mM TG); the fate of LPL-derived 3H-labeled fatty acids was split eve

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17

Loncar, Goran, Susann Fülster, Stephan von Haehling, and Vera Popovic. "Metabolism and the heart: An overview of muscle, fat, and bone metabolism in heart failure." International Journal of Cardiology 162, no. 2 (January 2013): 77–85. http://dx.doi.org/10.1016/j.ijcard.2011.09.079.

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18

Lopaschuk, Gary D., Qutuba G. Karwi, Rong Tian, Adam R. Wende, and E. Dale Abel. "Cardiac Energy Metabolism in Heart Failure." Circulation Research 128, no. 10 (May 14, 2021): 1487–513. http://dx.doi.org/10.1161/circresaha.121.318241.

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Alterations in cardiac energy metabolism contribute to the severity of heart failure. However, the energy metabolic changes that occur in heart failure are complex and are dependent not only on the severity and type of heart failure present but also on the co-existence of common comorbidities such as obesity and type 2 diabetes. The failing heart faces an energy deficit, primarily because of a decrease in mitochondrial oxidative capacity. This is partly compensated for by an increase in ATP production from glycolysis. The relative contribution of the different fuels for mitochondrial ATP produ

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19

Sherry, A. D., C. R. Malloy, R. E. Roby, A. Rajagopal, and F. M. Jeffrey. "Propionate metabolism in the rat heart by 13C n.m.r. spectroscopy." Biochemical Journal 254, no. 2 (September 1, 1988): 593–98. http://dx.doi.org/10.1042/bj2540593.

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High-resolution 13C n.m.r. spectroscopy has been used to examine propionate metabolism in the perfused rat heart. A number of tricarboxylic acid (TCA) cycle intermediates are observable by 13C n.m.r. in hearts perfused with mixtures of pyruvate and propionate. When the enriched 13C-labelled nucleus originates with pyruvate, the resonances of the intermediates appear as multiplets due to formation of multiply-enriched 13C-labelled isotopomers, whereas when the 13C-labelled nucleus originates with propionate, these same intermediates appear as singlets in the 13C spectrum since entry of propiona

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20

Broderick, Tom L. "Whole-body heat shock protects the ischemic rat heart by stimulating mitochondria respiration." Canadian Journal of Physiology and Pharmacology 84, no. 8-9 (September 2006): 929–33. http://dx.doi.org/10.1139/y06-039.

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Whole-body heat shock (HS) leads to an enhancement of postischemic mechanical function and an improvement in glucose use by the rat heart. Here, we examine the effect of HS on isolated mitochondrial metabolism during reperfusion in the working rat heart. Rats were anesthetized, and their body temperature was raised to 41–42 °C for 15 min. Control rats were treated the same way but were not exposed to hyperthermia. Twenty-fours after HS or sham treatment, rats were reanesthetized and the hearts were removed for perfusion with Krebs–Henseleit buffer, containing 11 mmol glucose/L and 1.2 mmol pal

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21

Evans, Rhys D. "Myocardial substrate metabolism in heart disease." Frontiers in Bioscience S4, no. 2 (2012): 556–80. http://dx.doi.org/10.2741/s285.

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22

Choy, Patrick C., Khai Tran, Grant M. Hatch, and Edwin A. Kroeger. "Phospholipid metabolism in the mammalian heart." Progress in Lipid Research 36, no. 2-3 (September 1997): 85–101. http://dx.doi.org/10.1016/s0163-7827(97)00005-2.

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23

ZAOBORNYJ, Tamara, Dar韔 E. IGLESIAS, Silvina S. BOMBICINO, Alberto BOVERIS, and Laura B. VALDEZ. "Nitric oxide metabolism in heart mitochondria." BIOCELL 40, no. 1 (2016): 55–58. http://dx.doi.org/10.32604/biocell.2016.40.055.

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24

Heather, Lisa C., and Kieran Clarke. "Metabolism, hypoxia and the diabetic heart." Journal of Molecular and Cellular Cardiology 50, no. 4 (April 2011): 598–605. http://dx.doi.org/10.1016/j.yjmcc.2011.01.007.

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25

Ascuitto, Robert J., and Nancy T. Ross-Ascuitto. "Substrate metabolism in the developing heart." Seminars in Perinatology 20, no. 6 (December 1996): 542–63. http://dx.doi.org/10.1016/s0146-0005(96)80068-1.

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26

Portman, Michael A. "Thyroid Hormone Regulation of Heart Metabolism." Thyroid 18, no. 2 (February 2008): 217–25. http://dx.doi.org/10.1089/thy.2007.0257.

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27

Lopaschuk, Gary D., and William C. Stanley. "Glucose Metabolism in the Ischemic Heart." Circulation 95, no. 2 (January 21, 1997): 313–15. http://dx.doi.org/10.1161/01.cir.95.2.313.

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28

Kawaguchi, H., H. Sano, K. Iizuka, H. Okada, T. Kudo, K. Kageyama, S. Muramoto, T. Murakami, H. Okamoto, and N. Mochizuki. "Phosphatidylinositol metabolism in hypertrophic rat heart." Circulation Research 72, no. 5 (May 1993): 966–72. http://dx.doi.org/10.1161/01.res.72.5.966.

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29

Seguro, Luis F. B. C., Rosa M. R. Pereira, Luciana P. C. Seguro, Valeria F. Caparbo, Monica S. Avila, Sandrigo Mangini, Iascara W. Campos, Fabio A. Gaiotto, Fabiana G. Marcondes-Braga, and Fernando Bacal. "Bone Metabolism Impairment in Heart Transplant." Transplantation 104, no. 4 (April 2020): 873–80. http://dx.doi.org/10.1097/tp.0000000000002906.

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30

Kawaguchi, H. "Polyphosphoinositide metabolism in hypertrophic rat heart." Journal of Molecular and Cellular Cardiology 24, no. 9 (September 1992): 1003–10. http://dx.doi.org/10.1016/0022-2828(92)91866-4.

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31

O'Brien, Terrence X. "Iron Metabolism, Anemia, and Heart Failure." Journal of the American College of Cardiology 58, no. 12 (September 2011): 1252–53. http://dx.doi.org/10.1016/j.jacc.2011.03.060.

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32

Karwi, Qutuba G., Dipsikha Biswas, Thomas Pulinilkunnil, and Gary D. Lopaschuk. "Myocardial Ketones Metabolism in Heart Failure." Journal of Cardiac Failure 26, no. 11 (November 2020): 998–1005. http://dx.doi.org/10.1016/j.cardfail.2020.04.005.

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33

Wescott, Andrew P., W. J. Lederer, and George S. B. Williams. "Excitation-Metabolism Coupling in Mouse Heart." Biophysical Journal 108, no. 2 (January 2015): 570a. http://dx.doi.org/10.1016/j.bpj.2014.11.3117.

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34

Lopaschuk, Gary D., Qutuba G. Karwi, Kim L. Ho, Simran Pherwani, and Ezra B. Ketema. "Ketone metabolism in the failing heart." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1865, no. 12 (December 2020): 158813. http://dx.doi.org/10.1016/j.bbalip.2020.158813.

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35

Houtkooper, R. H., and F. M. Vaz. "Cardiolipin, the heart of mitochondrial metabolism." Cellular and Molecular Life Sciences 65, no. 16 (April 21, 2008): 2493–506. http://dx.doi.org/10.1007/s00018-008-8030-5.

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36

Cavaliere, Franco, Mario Sciarra, Roberto Zamparelli, Carolina Monaco, Sabrina Bonifazi, and Rocco Schiavello. "Magnesium metabolism in open-heart surgery." Resuscitation 13, no. 4 (July 1986): 215–21. http://dx.doi.org/10.1016/0300-9572(86)90075-4.

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37

Soffia, Francisca, and Mario Penna. "Ethanol metabolism by rat heart homogenates." Alcohol 4, no. 1 (January 1987): 45–48. http://dx.doi.org/10.1016/0741-8329(87)90059-0.

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38

Herman, R. Peter, R. Scott Heller, Christopher M. Canavan, and Ceil A. Herman. "Leukotriene C4 action and metabolism in the isolated perfused bullfrog heart." Canadian Journal of Physiology and Pharmacology 66, no. 7 (July 1, 1988): 980–84. http://dx.doi.org/10.1139/y88-161.

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The effects of leukotrienes (LTs) have been widely studied in the isolated perfused mammalian heart; however, little is known about the effect or metabolism of LTs in the isolated bullfrog heart. Isolated perfused bullfrog hearts were administered randomized doses of LTC4, LTD4, or LTE4. The cardiac parameters of heart rate, developed tension, and its first derivative (dT/dt) were recorded. LTC4 was the most potent of the leukotrienes tested in eliciting positive inotropic effects. LTD4 and LTE4 were equally effective but about one order of magnitude less potent than LTC4. None of the LTs show

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39

Abozguia, K., G. Shivu, I. Ahmed, T. Phan, and M. Frenneaux. "The Heart Metabolism: Pathophysiological Aspects in Ischaemia and Heart Failure." Current Pharmaceutical Design 15, no. 8 (March 1, 2009): 827–35. http://dx.doi.org/10.2174/138161209787582101.

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40

Rumsey, W. L., L. Kilpatrick, D. F. Wilson, and M. Erecinska. "Myocardial metabolism and coronary flow: effects of endotoxemia." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (December 1, 1988): H1295—H1304. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1295.

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The effects of sublethal endotoxemia on the regulation of coronary flow by myocardial metabolism were examined in the isolated perfused heart preparation. Fasted Sprague-Dawley rats were injected (ip) with either endotoxin (0.5 mg/kg of body wt) or 5% dextrose 12 h before heart perfusion. The efficacy of endotoxin treatment was determined by measurement of plasma [NH3] and [urea] and colonic temperature. During perfusion with buffer containing glucose-pyruvate, oxygen consumption and coronary flow were increased by 17 and 42%, respectively, in hearts from endotoxin-treated rats as compared wit

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41

Chung, Youngran. "Myocardial Po2 does not limit aerobic metabolism in the postischemic heart." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 2 (January 15, 2016): H226—H238. http://dx.doi.org/10.1152/ajpheart.00335.2015.

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Reperfused hypertrophic hearts are prone to develop reflow abnormalities, which are likely to impair O2 return to the myocardium. Yet, reflow deficit may not be the only factor determining postischemic oxygenation in the hypertrophic heart. Altered O2 demand may also contribute to hypoxia. In addition, the extent to which myocardial Po2 dictates energy and functional recovery in the reperfused heart remains uncertain. In the present study, moderately hypertrophied hearts from spontaneously hypertensive rats were subjected to ischemia-reperfusion, and the recovery time courses of pH and high-en

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42

Stenbit, Antine E., Ellen B. Katz, John C. Chatham, David L. Geenen, Stephen M. Factor, Robert G. Weiss, Tsu-Shuen Tsao, et al. "Preservation of glucose metabolism in hypertrophic GLUT4-null hearts." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 1 (July 1, 2000): H313—H318. http://dx.doi.org/10.1152/ajpheart.2000.279.1.h313.

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GLUT4-null mice lacking the insulin-sensitive glucose transporter are not diabetic but do exhibit abnormalities in glucose and lipid metabolism. The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy. GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. However, GLUT4-null mice have normal blood pressure and maintain a normal cardiac contractile protein profile. Unexpectedly, although they lack the predominant glucose transporter in the heart, GLUT4-null hearts transport glucose and synthesize glycogen at normal levels, but gene express

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43

Robishaw, J. D., and J. R. Neely. "Coenzyme A metabolism." American Journal of Physiology-Endocrinology and Metabolism 248, no. 1 (January 1, 1985): E1—E9. http://dx.doi.org/10.1152/ajpendo.1985.248.1.e1.

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The metabolism of coenzyme A and control of its synthesis are reviewed. Pantothenate kinase is an important rate-controlling enzyme in the synthetic pathway of all tissues studied and appears to catalyze the flux-generating reaction of the pathway in cardiac muscle. This enzyme is strongly inhibited by coenzyme A and all of its acyl esters. The cytosolic concentrations of coenzyme A and acetyl coenzyme A in both liver and heart are high enough to totally inhibit pantothenate kinase under all conditions. Free carnitine, but not acetyl carnitine, deinhibits the coenzyme A-inhibited enzyme. Carni

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44

Sambandam, Nandakumar, Mohammed A. Abrahani, Scott Craig, Osama Al-Atar, Esther Jeon, and Brian Rodrigues. "Metabolism of VLDL is increased in streptozotocin-induced diabetic rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (June 1, 2000): H1874—H1882. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1874.

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In streptozotocin (STZ)-induced diabetic rats, we previously showed an increased heparin-releasable (luminal) lipoprotein lipase (LPL) activity from perfused hearts. To study the effect of this enlarged LPL pool on triglyceride (TG)-rich lipoproteins, we examined the metabolism of very-low-density lipoprotein (VLDL) perfused through control and diabetic hearts. Diabetic rats had elevated TG levels compared with control. However, fasting for 16 h abolished this difference. When the plasma lipoprotein fraction of density <1.006 g/ml from fasted control and diabetic rats was incubated in vitro

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45

NGIMBOUS, BEDEL BIYIHA, FRANCINE BOURGEOIS, CHRISTOPHE MAS, MICHEL SIMONNEAU, and JEAN-MARIE MOALIC. "Heart transplantation changes the expression of distinct gene families." Physiological Genomics 7, no. 2 (December 21, 2001): 115–26. http://dx.doi.org/10.1152/physiolgenomics.00013.2001.

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We took advantage of the combination of a rat heart transplantation model with a modified differential display RT-PCR method to identify transcriptome changes in the right atria from transplanted compared with native hearts. Based on sequence homology search, the 37 cDNAs differentially displayed both 2 and 7 days posttransplantation were categorized into 7 unknown transcripts, 16 expressed sequence tags (ESTs), and 14 partially or completely characterized genes. The last group cDNAs, validated by relative RT-PCR, belonged to diverse gene families involved in specific metabolisms, protein synt

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46

Wang, Xin, David G. Hole, Teresa H. M. Da Costa, and Rhys D. Evans. "Alterations in myocardial lipid metabolism during lactation in the rat." American Journal of Physiology-Endocrinology and Metabolism 275, no. 2 (August 1, 1998): E265—E271. http://dx.doi.org/10.1152/ajpendo.1998.275.2.e265.

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Metabolism of nonesterified fatty acid (palmitate, 1.1 mM) and triacylglycerol (TAG; triolein, 0.4 mM in the form of both rat chylomicrons and very low density lipoproteins) was studied in isolated perfused working hearts from fed nulliparous, lactating, and weaned rats. Hearts from virgin rats oxidized palmitate readily, but optimal cardiac mechanical performance occurred during perfusion with chylomicrons. In hearts from lactating dams, there was a significant increase in palmitate oxidation and a marked decrease in TAG oxidation from both chylomicrons and very low density lipoproteins compa

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47

Raut, Robert, Jean-Lucien Rouleau, Charles Blais, Hugues Gosselin, Giuseppe Molinaro, Martin G. Sirois, Yves Lepage, Philippe Crine, and Albert Adam. "Bradykinin metabolism in the postinfarcted rat heart: role of ACE and neutral endopeptidase 24.11." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 5 (May 1, 1999): H1769—H1779. http://dx.doi.org/10.1152/ajpheart.1999.276.5.h1769.

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The respective role of angiotensin-converting enzyme (ACE) and neutral endopeptidase 24.11 (NEP) in the degradation of bradykinin (BK) has been studied in the infarcted and hypertrophied rat heart. Myocardial infarction (MI) was induced in rats by left descendant coronary artery ligature. Animals were killed, and hearts were sampled 1, 4, and 35 days post-MI. BK metabolism was assessed by incubating synthetic BK with heart membranes from sham hearts and infarcted (scar) and noninfarcted regions of infarcted hearts. The half-life ( t ½) of BK showed significant differences among the three types

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48

Kärkkäinen, Olli, Tomi Tuomainen, Maija Mutikainen, Marko Lehtonen, Jorge L. Ruas, Kati Hanhineva та Pasi Tavi. "Heart specific PGC-1α deletion identifies metabolome of cardiac restricted metabolic heart failure". Cardiovascular Research 115, № 1 (20 червня 2018): 107–18. http://dx.doi.org/10.1093/cvr/cvy155.

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Abstract Aims Heart failure (HF) is associated with drastic changes in metabolism leading to a cardiac energy deficiency well as maladaptive changes in multiple other tissues. It is still unclear which of these changes originates from cardiomyocyte metabolic remodelling or whether they are induced secondarily by systemic factors. Our aim here was to induce cardiac restricted metabolic changes mimicking those seen in HF and to characterize the associated metabolite changes in the heart, circulation, and peripheral tissues. Methods and results We generated a cardiac specific PGC-1α knockout mice

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49

Suleymanlar, G., H. Z. Zhou, M. McCormack, N. Elkins, R. Kucera, O. K. Reiss, and J. I. Shapiro. "Mechanism of impaired energy metabolism during acidosis: role of oxidative metabolism." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 6 (June 1, 1992): H1818—H1822. http://dx.doi.org/10.1152/ajpheart.1992.262.6.h1818.

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Isolated perfused rat hearts were used to study the effects of metabolic acidosis on energy metabolism. Hearts perfused with different substrates (glucose, pyruvate, and succinate) were subjected to metabolic acidosis. With all substrates, there were comparable decrements in oxygen consumption (approximately 35%), cardiac function (decrease in first derivative of pressure of 65%), and similar changes in high-energy phosphates (approximately 150% increases in inorganic phosphate and 25% decreases in phosphocreatine concentrations) with metabolic acidosis. To further investigate the metabolic ef

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Akasheva, D. U., I. A. Pokshubina, E. A. Plokhova, and О. N. Tkacheva. "CARBOHYDRATE METABOLISM DISORDERS IN THE HEART AGEING." Cardiovascular Therapy and Prevention 16, no. 3 (January 1, 2017): 81–86. http://dx.doi.org/10.15829/1728-8800-2017-3-81-86.

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