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Journal articles on the topic 'Heart Metabolism'

To see the other types of publications on this topic, follow the link: Heart Metabolism.

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 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 palmitate. Although the absolute values obtained for glycolysis and glucose oxidation and fatty acid oxidation are significantly higher than those reported for rat hearts, the pattern of substrate metabolism in mouse hearts is similar to that observed in hearts from larger mammals. The metabolism of mouse hearts can be altered by fatty acid concentration in a manner similar to that observed in larger animals; increasing palmitate concentration altered the balance of substrate metabolism to increase overall energy derived from fatty acids from 64 to 92%.

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 for the differences in the accumulation of LPC in the microsomal membrane of different animal species was investigated. Our results strongly indicate that the LPC level in the microsomal membrane may be regulated by the activity of microsomal lysophospholipase.

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. Left ventricular developed pressure (LVDP = LVSP - LVEDP) and pressure-rate product (LVDP × HR) were calculated. Coronary effluent was collected to measure flow and metabolites. Heart tissue samples were collected for metabolite analysis. Results: DOB increased HR, LVEDP and the pressure-rate product [LVDP × HR]. Mean lactate production increased in DOB, but not in SAL control hearts, and was correlated with heart acylcarnitine, but not with coronary flow. Tissue acylcarnitine levels were higher in the DOB than in the SAL group. Plasma total carnitine was correlated with [LVDP × HR] and LVDP, but not with HR. The findings demonstrate that DOB alters myocardial carnitine metabolism and suggest that carnitine status may affect cardiac response to inotropic agents.Key words: carnitine, dobutamine, neonate, swine, isolated perfused heart.

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 non-esterified fatty acids has been extensively investigated in the perfused rat heart, but fatty acids may also be derived from circulating triacylglycerols (TAG) in lipoproteins [chylomicrons, very-low-density-lipoprotein (VLDL)]. TAG requires initial hydrolysis by the endothelial enzyme lipoprotein lipase and hence an intact heart preparation is vital to maintain tissue structural integrity. Chylomicron-TAG utilization and fate (oxidation, tissue-lipid deposition) in isolated working hearts has been studied using chylomicrons obtained from thoracic-duct catheters. However, lack of availability of sufficient quantities of VLDL has hindered examination of their cardiac utilization; the recent development of a technique to produce large quantities of radiolabelled rat VLDL has facilitated these studies and established that VLDL-TAG is an important metabolic substrate for working heart. Results relating to myocardial utilization of VLDL-TAG under varying physiological (lactation) and pathological (endotoxinaemia) conditions will be presented. The putative role of VLDL as a regulator of cardiac lipid metabolism will also be discussed.

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 evenly between oxidation (production of3H2O) and esterification (incorporation into tissue lipids, mainly TG). In comparison, the oxidation of 0.4 mM [3H]palmitate complexed to albumin was fourfold greater than esterification into tissue lipids. Surprisingly, the addition of unlabeled palmitate (0.4 or 1.2 mM) to perfusions with3H-chylomicrons did not affect the fate (either oxidation or esterification) of LPL-derived 3H-fatty acids. These results suggest that fatty acids produced from lipoprotein hydrolysis by the action of LPL and fatty acids from a fatty acid-albumin complex do not enter a common metabolic pool in the heart.

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 production also changes, including a decrease in glucose and amino acid oxidation, and an increase in ketone oxidation. The oxidation of fatty acids by the heart increases or decreases, depending on the type of heart failure. For instance, in heart failure associated with diabetes and obesity, myocardial fatty acid oxidation increases, while in heart failure associated with hypertension or ischemia, myocardial fatty acid oxidation decreases. Combined, these energy metabolic changes result in the failing heart becoming less efficient (ie, a decrease in cardiac work/O 2 consumed). The alterations in both glycolysis and mitochondrial oxidative metabolism in the failing heart are due to both transcriptional changes in key enzymes involved in these metabolic pathways, as well as alterations in NAD redox state (NAD + and nicotinamide adenine dinucleotide levels) and metabolite signaling that contribute to posttranslational epigenetic changes in the control of expression of genes encoding energy metabolic enzymes. Alterations in the fate of glucose, beyond flux through glycolysis or glucose oxidation, also contribute to the pathology of heart failure. Of importance, pharmacological targeting of the energy metabolic pathways has emerged as a novel therapeutic approach to improving cardiac efficiency, decreasing the energy deficit and improving cardiac function in the failing heart.

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 propionate into the TCA cycle occurs via succinyl-CoA. An analysis of the isotopomer populations in hearts perfused with [3-13C]pyruvate plus unlabelled propionate indicates that about 27% of the total pyruvate pool available to the heart is derived directly from unlabelled propionate. This was substantiated by perfusing a heart for 2 h with [3-13C]propionate as the only available exogenous substrate. Under these conditions, all of the propionate consumed by the heart, as measured by conventional chemical analysis, ultimately entered the oxidative pathway as [2-13C] or [3-13C]pyruvate. This is consistent with entry of propionate into the TCA cycle intermediate pools as succinyl-CoA and concomitant disposal of malate to pyruvate via the malic enzyme. 13C resonances arising from enriched methylmalonate and propionylcarnitine are also detected in hearts perfused with [3-13C] or [1-13C]propionate which suggests that 13C n.m.r. may be useful as a non-invasive probe in vivo of metabolic abnormalities involving the propionate pathway, such as methylmalonic aciduria or propionic acidaemia.

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 palmitate/L prebound to 3% albumin. Hearts were subjected to 25 min of global ischemia followed by 30 min of reperfusion. At the end of reperfusion, heart mitochondria were isolated using differential centrifugation and respiration measured in the presence of pyruvate, glutamate, or palmitoylcarnitine. Hearts subjected to HS showed an enhanced recovery of function, expressed as aortic flow, during the reperfusion period, compared with sham hearts. This improved functional status was associated with a significant increase in state 3 respiration in the presence of pyruvate, glutamate, or palmitoylcarnitine. These results show that HS offers protection against ischemic damage, and that a possible mechanism might be the enhanced myocardial metabolism of fuels.

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 showed any chronotropic effects in this preparation. A series of [3H]LTC4 metabolism experiments were carried out using whole perfused hearts and minced bullfrog heart tissue. Isolated perfused bullfrog hearts administered [3H]LTC4 converted significant amounts to [3H]LTD4, and to a lesser degree, [3H]LTE4, during the 6-min course of collection. Both minced atrial and ventricular tissue converted [3H]LTC4 to radioactive metabolites that co-migrated with authentic LTD4 and LTE4 standards. In both tissues, the major product was [3H]LTD4, with smaller amounts of [3H]LTE4 produced. The atrium converted significantly more [3H]LTC4 to its metabolites than did the ventricle. The metabolism of [3H]LTC4 to [3H]LTD4 by both tissues was virtually abolished in the presence of serine borate. Cysteine had no effect on [3H]LTE4 production. The data in this study demonstrate that leukotrienes have the opposite inotropic effect on the heart when compared with mammals. Also in contrast to mammals, frogs metabolize LTC4 to a less potent compound and may use the LTC4 to LTD4 conversion as a mechanism of LTC4 inactivation.

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 with those from controls. In the hearts from endotoxemic animals, the mitochondrial [NAD+]/[NADH] was decreased by approximately 25%, and the active form of pyruvate dehydrogenase was increased by 36% as compared with control hearts. [ATP]f/[ADP]f[Pi] was unaltered. The enhanced metabolic rate was associated with comparable changes in peak systolic pressure development, maximal positive and negative dP/dt, and the tension-time index when measured in the isovolumetric preparation. In these hearts, stimulation of respiration by perfusion with an alternate source of fuel or inhibition by infusion of amytal elicited large, transient increases in the level of coronary flow that returned rapidly to prestimulus values. By contrast, in hearts from controls, the transient increase in flow was coupled to sustained vasodilation, i.e., approximately 30% rise in flow for either metabolic condition. In both groups, [ATP]f/[ADP]f[Pi] either increased or decreased with stimulation or inhibition of respiration, respectively. Adenosine (1.2 microM) produced a 35% increase in flow in the hearts from the control animals, whereas it was without significant effect in those from the endotoxin-treated animals. It is concluded that sublethal endotoxemia causes 1) an increased metabolic rate and enhanced mechanical activity in the heart and 2) an uncoupling of flow from regulation by cardiac metabolism.

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-energy phosphates were followed by 31P NMR. 1H NMR measurement of intracellular myoglobin assessed tissue O2 levels. The present study found that the exacerbation of hypoxia in the postischemic spontaneously hypertensive rat heart arises mostly from impaired microvascular supply of O2. However, postischemic myocardial Po2, at least when it exceeds ∼18% of the preischemic level, does not limit mitochondrial respiration and high-energy phosphate resynthesis. It only passively reflects changes in the O2 supply-demand balance.

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 expression of rate-limiting enzymes involved in fatty acid oxidation is decreased. The GLUT4-null heart represents a unique model of hypertrophy that may be used to study the consequences of altered substrate utilization in normal and pathophysiological conditions.

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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. Carnitine alone does not increase enzyme activity. Thus changes in the acetyl carnitine-to-carnitine ratio that occur with nutritional states provides a mechanism for regulation of coenzyme A synthetic rates. Changes in the rate of coenzyme A synthesis in liver and heart occurs with fasting, refeeding, and diabetes and in heart muscle with hypertrophy. The pathway and regulation of coenzyme A degradation are not understood.

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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 with purified bovine or rat LPL, VLDL from diabetic animals was hydrolyzed as proficiently as VLDL from control animals. Post-heparin plasma lipolytic activity was comparable in control and diabetic animals. However, perfusion of control and diabetic rats with heparinase indicated that diabetic hearts had larger amounts of LPL bound to heparan sulfate proteoglycan-binding sites. [3H]VLDL obtained from control rats, when recirculated through the isolated heart, disappeared at a significantly faster rate from diabetic than from control rat hearts. This increased VLDL-TG hydrolysis was essentially abolished by prior perfusion of the diabetic heart with heparin, implicating LPL in this process. These findings suggest that the enlarged LPL pool in the diabetic heart is present at a functionally relevant location (at the capillary lumen) and is capable of hydrolyzing VLDL. This could increase the delivery of free fatty acid to the heart, and the resultant metabolic changes could induce the subsequent cardiomyopathy that is observed in the chronic diabetic rat.

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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 synthesis, cell signaling, and transcription. Furthermore, we identified differential transcripts corresponding to denervation and fetal gene reexpression. We found coordinate downregulation of genes involved in energy metabolism and protein synthesis regulation, similar to that reported for senescent skeletal muscle. From these transcriptome changes, we propose that heart transplants and senescent muscles share common molecular mechanisms.

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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 compared with hearts from nulliparous animals. There was a concomitant decrease in lipoprotein lipase activity in hearts from lactating animals, and TAG in the absence of palmitate could not support optimal cardiac mechanical function. After litter removal, the changes in fatty acid and TAG metabolism observed in lactation returned to nulliparous values within 96 h. These results suggest that, during lactation, both exogenous and endogenous TAGs are directed away from heart and toward the lactating mammary gland; the heart, therefore, has to rely to a greater extent on nonesterified fatty acid for energy provision under these conditions.

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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 of tissue at 4 days [sham heart (114 ± 7 s) > noninfarcted region (85 ± 4 s) > infarcted region (28 ± 2 s)] and 35 days post-MI [sham heart (143 ± 6 s) = noninfarcted region (137 ± 9 s) > infarcted region (55 ± 4 s)]. No difference was observed at 1 day post-MI. The participation of ACE and NEP in the metabolism of BK was defined by preincubation of the membrane preparations with enalaprilat, an ACE inhibitor, and omapatrilat, a vasopeptidase inhibitor that acts by combined inhibition of NEP and ACE. Enalaprilat significantly prevented the rapid degradation of BK in every tissue type and at every sampling time. Moreover, omapatrilat significantly increased the t ½ of BK compared with enalaprilat in every tissue type and at every sampling time. These results demonstrate that experimental MI followed by left ventricular dysfunction significantly modifies the metabolism of exogenous BK by heart membranes. ACE and NEP participate in the degradation of BK since both enalaprilat and omapatrilat have potentiating effects on the t ½ of BK.

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Kärkkäinen, Olli, Tomi Tuomainen, Maija Mutikainen, Marko Lehtonen, Jorge L. Ruas, Kati Hanhineva, and Pasi Tavi. "Heart specific PGC-1α deletion identifies metabolome of cardiac restricted metabolic heart failure." Cardiovascular Research 115, no. 1 (June 20, 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 (KO) to specifically induce metabolic dysregulation typically accompanied by HF and performed a non-targeted LC-MS metabolite profiling analysis of heart, plasma, liver, and skeletal muscle to identify metabolites associated with cardiac specific metabolic remodelling. The KO animals developed a progressive cardiomyopathy with cardiac dilatation leading to fatal HF. At 17 weeks of age, when significant remodelling had occurred but before the onset of HF, isolated PGC-1α deficient cardiomyocytes had suppressed glucose and fatty acid oxidation as well as blunted anaerobic metabolism. KO hearts displayed a distinctive metabolite profile with 92 significantly altered molecular features including metabolite changes in energy metabolism, phospholipid metabolism, amino acids, and oxidative stress signalling. Some of the metabolite changes correlated with the specific parameters of cardiac function. We did not observe any significant alterations in the metabolomes of the other measured tissues or in plasma. Conclusions Heart specific PGC-1α KO induces metabolic, functional, and structural abnormalities leading to dilating cardiomyopathy and HF. The metabolic changes were limited to the cardiac tissue indicating that cardiomyocyte metabolic remodelling is not sufficient to evoke the body wide metabolic alterations usually associated with HF.

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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 effects of acidosis, isolated cardiac mitochondria were exposed to different incubation media pH conditions and given simple metabolites (glutamate/malate, succinate, or pyruvate) or fatty acids (octanoate). Reduction of incubation media pH to 6.0 did not significantly affect either coupled respiration rate or the respiratory control ratio (RCR) with any substrate. These data suggest that metabolic acidosis induces decreases in energy production in the isolated perfused heart by inhibiting mitochondrial substrate utilization and not by impairing glycolysis. However, this impairment of mitochondrial function is not a direct effect of acidosis itself but appears to occur secondarily to some other effects of acidosis which are, as yet, incompletely understood.

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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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