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Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Heart Metabolism.'
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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.
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%.
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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.
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.
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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.
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.
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.
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.
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.
Dissertations / Theses on the topic "Heart Metabolism":
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Murray, Andrew James. "Control of cardiac metabolism and efficiency." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:858cc1f9-7ba0-4999-a1c8-614a950888c2.
Babić, Nikolina. "Regulation of energy metabolism of heart myoblasts /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/11563.
Belke, Darrell David. "Hypothermia and energy substrate metabolism in the heart." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21548.pdf.
Råmunddal, Truls Are. "Myocardial metabolism in experimental infarction and heart failure /." Göteborg : Department of Molecular and Clinical Medicine, The Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy Göteborg University, 2008. http://hdl.handle.net/2077/9565.
Heather, Lisa Claire. "Substrate transporters and metabolism in the hypertrophied heart." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442468.
Beadle, Roger. "Metabolic manipulation in chronic heart failure." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=201651.
Treatments aimed at modifying cardiac substrate utilisation are designed to improve metabolic efficiency. In the fasting state, the heart mainly relies on fatty acid oxidation for its energy production. The heart can adapt to metabolise glucose, lactate and amino acids depending on the predominate milieu and demands placed upon it. A shift from fatty acid oxidation to carbohydrate oxidation leads to a lower oxygen consumption per unit of adenosine triphosphate produced. It is this concept of improving cardiac efficiency by a reduction in oxygen demand that underpins the use of metabolic manipulating agents as a therapeutic strategy in heart failure. Cardiac energy starvation is increasingly recognised as playing a central role in the pathophysiology of heart failure. Alterations in substrate utilisation thus underlie the hope that metabolic manipulating agents will be of benefit in heart failure of both ischaemic and non-ischaemic origin. This metabolic shift is achieved by promoting glucose utilisation and reducing the utilisation of fatty acids. This leads to a greater production of adenosine triphosphate per unit of oxygen consumed. With an ongoing demand for treatment options in ischaemic heart disease and the growing burden of chronic heart failure, new treatment modalities beyond contemporary therapy warrant consideration. This thesis aims to investigate the short term effects of metabolic manipulation on changes in cardiac energetic status, cardiac function, efficiency and substrate utilisation.
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Adix, Longlet Nancy J. "Chronic Ventricular Sympathectomy : Effects on Myocardial Metabolism." Thesis, University of North Texas, 1993. https://digital.library.unt.edu/ark:/67531/metadc278768/.
Chronic ventricular sympathectomy elicits changes in the coronary circulation, myocardial oxygen consumption and size of infarction resulting fromcoronary occlusion. These changes indicate a change occurring in the basic metabolism of the heart in response to the removal of its sympathetic nervous input. This hypothesis was tested using two groups of dogs, a shamoperated control and a ventricular sympathectomized group. The sympathectomy procedure was an intrapericardial surgical technique which selectively removes ventricular sympathetic input. Four weeks after surgery, left ventricular tissue samples were obtained and rapidly frozen to -80°C. Selected metabolic variables were then compared between the two groups.
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Jones, Barney. "Ischaemia and efficiency in the isolated heart." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311982.
Kalsi, Kameljit Kaur. "Nucleotide and adenosine metabolism in heart failure and cardioprotection." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409176.
Dhalla, Naranjan S., Grant N. Pierce, and Robert E. Beamish, eds. Heart Function and Metabolism. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2053-1.
Sideman, S., and R. Beyar, eds. Activation, Metabolism and Perfusion of the Heart. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3313-2.
Van Der Vusse, Ger J., ed. Lipid Metabolism in Normoxic and Ischemic Heart. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1611-4.
van der Vusse, Ger J., and Hans Stam, eds. Lipid Metabolism in the Healthy and Disease Heart. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3514-0.
Stam, H., and G. J. van der Vusse, eds. Lipid metabolism in the normoxic and ischaemic heart. Heidelberg: Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-08390-1.
Pfister, Roman, and Erland Erdmann. "Heart Failure." In Metabolism of Human Diseases, 251–57. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-0715-7_37.
Slavich, Massimo, and Juan Carlos Kaski. "Atherosclerotic Heart Disease." In Metabolism of Human Diseases, 243–49. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-0715-7_36.
Kowaltowski, Alicia, and Fernando Abdulkader. "Metabolism and Heart Disease." In Where Does All That Food Go?, 117–23. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50968-2_11.
Kusmic, Claudia, and Serena L’Abbate. "TH Metabolism in Ischemia/Reperfusion Models." In Thyroid and Heart, 71–83. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36871-5_6.
Laughlin, Maren R. "Cardiac Glycogen Metabolism in Diabetes." In The Heart in Diabetes, 166–88. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1269-7_8.
Haugaard, N., M. E. Hess, A. Torbati, and O. L. Tulp. "Energy Metabolism in Diabetic Heart." In Developments in Cardiovascular Medicine, 199–208. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2051-7_15.
Kako, K. J., and M. Kato. "Phospholipid Metabolism in Heart Membranes." In Myocardial Ischemia, 99–112. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5_8.
Bogazzi, Fausto, and Daniele Cappellani. "Heart Drugs and Influences on TH Metabolism." In Thyroid and Heart, 311–25. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36871-5_23.
Conference papers on the topic "Heart Metabolism":
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Zhang, Yu, Wataru Mizushima, Shinichi Oka, Peiyong Zhai, and Dominic Del Re. "Abstract B19: Neurofibromin 2 regulates metabolism in the heart." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-b19.
Miller, JJ, YB Ding, D. Ball, AZ Lau, and DJ Tyler. "P9 Hyperpolarised ketone body metabolism in the rat heart." In British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.14.
Hundertmark, MJ, CT Rodgers, O. Rider, S. Neubauer, and M. Mahmod. "P21 Cardiac metabolism in patients with heart failure with mid-range ejection fraction." In British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.26.
Reutter, Bryan W., Rostyslav Boutchko, Ronald H. Huesman, Stephen M. Hanrahan, Kathleen M. Brennan, Anne C. Sauve, and Grant T. Gullberg. "Dynamic pinhole SPECT imaging and compartmental modeling of fatty acid metabolism in the rat heart." In 2008 IEEE Nuclear Science Symposium and Medical Imaging conference (2008 NSS/MIC). IEEE, 2008. http://dx.doi.org/10.1109/nssmic.2008.4774275.
Vyas, R., H. Cheng, P. E. Grant, J. Newburger, K. Hagan, M. A. Franceschini, and M. Dehaes. "Lower Cerebral Oxygen Metabolism In Neonates With Congenital Heart Disease As Compared To Healthy Neonates." In Biomedical Optics. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/biomed.2014.bm3a.19.
Reutter, B. W., R. Boutchko, R. H. Huesman, A. C. Sauve, and G. T. Gullberg. "Tissue spillover correction for dynamic pinhole SPECT studies of fatty acid metabolism in the rat heart." In 2009 IEEE Nuclear Science Symposium and Medical Imaging Conference (NSS/MIC 2009). IEEE, 2009. http://dx.doi.org/10.1109/nssmic.2009.5401782.
Kluza, J., V. Peugnet, W. Laine, G. Kervoaze, G. Remy, I. Wolowczuck, P. Gosset, et al. "Validation of a new strategy to maintain functional mitochondrial metabolism in conserved murine heart and lung tissues." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.10.
Terres, W., C. Hamm, W. Kupper, and W. Bleifeld. "PLATELET AGGREGABLLITY AND METABOLISM IN PATIENTS WITH UNSTABLE ANGINA PECTORIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643777.
Several platelet products indicating platelet activation have been detected in blood and urine of patients (PTS) with angina pectoris (AP) at rest. Platelet activation mainly depends on local changes in the morphology or biochemical behaviour of the vessels. Whether platelet hyperaggregability is of additional importance in the pathogenesis of unstable AP is up to now unclear. In a prospective trial we therefore evaluated 32 patients (PTS) with coronary heart disease, 16 with AP at rest during the last 8 hours before blood collection and 16 age and sex matched controls with stable exertional AP. Platelet aggregation was measured upon stimulation with ADP (0.5, 1 and 10 μmol/l) and collagen (1and 5μg/ml), and c-AMP was determined in platelet rich plasma before, and, as an estimate of platelet adenylate cyclase activity, after stimulation of this enzyme with PGE 1 (10 μmol/l for 30 s). For all concentrations of both ADP and collagen no significant differences in the rates and extents of aggregation could be found between the groups. Correspondingly, the mean (±. 2 SEM) concentrations of c-AMP were similar, basally (4.1 ±.1.4 pmol/ml for PTS withunstable AP and 5.3 t 1.3 pmol/ml for PTS with stable AP)and after stimulation of platelet adenylate cyclase with PGE 1 (14.8 ± 4.1 vs. 17.2 ± 2.8 pmol/ml).Conclusion: No generalized platelet hyperaggregability could be detected in our PTS with unstable AP when compared to controls with stable exertional AP.
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NIADA, R., R. Porta, R. Tettamanti, R. Pescador, M. Mantovani, and G. Prino. "DEFIBROTIDE IN EXPERIMENTAL MYOCARDIAL ISCHEMIA IN THE CAT: EFFECTS ON HEMODYNAMICS, ENERGY METABOLISM AND INFARCT SIZE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643152.
Defibrotide was able to prevent the hemodynamic and biochemical alterations caused by acute myocardial ischemia (AMI) induced by coronary occlusion in the cat when infused 3.5 h before and 5 h after left anterior descending coronary artery (LAD) occlusion. In the platelet perfused heart, Defibrotide was a selective stimulator of coronary vascular PGI^ but not of platelet thromboxane formation. The present study was designed both to investigate the effects of Defibrotide injected 30 min after the induction of acute myocardial ischemia (AMI) in the cat and to evaluate the ability of this drug to reduce infarct size. In the first set of experiments a permanent ligature (5 hours) was placed around LAD. ST segment from ECG, mean aortic pressure (MAP), heart rate (HR) and the pressure-heart rate index (PRI) were considered. Plasma and tissue creatine phosphckinase activity (CFK), tissue lactate and ATP were measured by enzymatic kits from Boehringer Biochemia. 30 min after coronary occlusion a loading dose of Defibrotide (32 ng Kg-1 ) was administered i.v. immediately followed by an infusion (32 ng Kg-1 h 4.5 h-1) MAP, HR and PRI were not modified either by AMI or by the infusion of Defibrotide. AMI-ST segment increases were reduced by Defibrotide from 0.5 h after the beginning of the treatment (—49% vs. AMI control) to the and of experiments (-83% vs. AMI control after 5 h occlusion period). Plasma CFK was reduced from 2.5 h after the beginning of the treatment (-29%) till the end of experiments (-52%). Ischemic tissue CFK, lactate and ATP were normalized by Defibrotide. In the second set of experiments the animals were infused with Defibrotide (50 or 200 mg Kg-1 h-1 , i.v.) starting 2 hours before coronary ligature. The infusion was maintained throughout the 5 h occlusion period. The risk and infarct areas were measured by Evans blu and nitroblue tetrazoliun staining. The 51 ± 3% of risk area was infarcted in AMI control cats. Defibrotide at the two tested doses significantly reduced these infarct areas to 42 ± 4% and 34 ± 2% of risk areas respectively. The beneficial effects of Defibrotide observed in AMI could be attributed both to its ability to enhance PGI2 release from vascular walls and to improved local tissue oxygenation and energy supplies. However it could be taken into account a direct cytoprotective action.
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Albuquerque-Neto, Cyro, and Jurandir Itizo Yanagihara. "A Passive Model of the Heat, Oxygen and Carbon Dioxide Transport in the Human Body." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11104.
The aim of this work is the development of a mathematical model which integrates a model of the human respiratory system and a model of the human thermal system. Both models were previously developed at the same laboratory, based on classical works. The human body was divided in 15 segments: head, neck, trunk, arms, forearms, hands, thighs, legs and feet. Those segments have the form of a cylinder (circular cross-section) or a parallelogram (hands and feet) with the following tissue layers: muscle, fat, skin, bone, brain, lung, heart and viscera. Two different geometries are used to model the transport of mass and heat in the tissues. For the mass transfer, those layers are considered as tissue compartments. For the heat transfer, the body geometry is taken into account. Each segment contains an arterial and a venous compartment, representing the large vessels. The blood in the small vessels are considered together with the tissues. The gases are transported by the blood dissolved and chemically reacted. Metabolism takes place in the tissues, where oxygen is consumed generating carbon dioxide and heat. In the lungs, mass transfer happens by diffusion between an alveolar compartment and several pulmonary capillaries compartments. The skin exchanges heat with the environment by convection, radiation and evaporation. The differential transport equations were obtained by heat and mass balances. The discretization heat equations were obtained applying the finite volume method. The regulation mechanisms were considered as model inputs. The results show three different environment situations. It was concluded that the gas transport is most influenced by the temperature effects on the blood dissociation curves and the metabolism rise in a cold environment by shivering.
Reports on the topic "Heart Metabolism":
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Andrews, Matthew T. Regulation of Genes Controlling Carbohydrate Metabolism in the Heart of a Hibernating Mammal. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada424253.
Research, Gratis. Brown Fat Activation: A Future Treatment for Obesity & Diabetes. Gratis Research, November 2020. http://dx.doi.org/10.47496/gr.blog.01.
Brown fat holds a promising therapeutic approach to prevent obesity and type 2 diabetes by its profound effects on body weight reduction, heat generation, increased insulin sensitivity and glucose metabolism regulation
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Upah, Nathan, Sarah Pearce, Nicholas K. Gabler, and Lance H. Baumgard. Effects of Heat Stress and Plane of Nutrition on Production and Metabolism in Growing Pigs. Ames (Iowa): Iowa State University, January 2011. http://dx.doi.org/10.31274/ans_air-180814-107.
Staab, Janet E., Margaret A. Kolka, and Bruce S. Cadarette. Metabolic Rate and Heat Stress Associated With Flying Military Rotary-Wing Aircraft. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/ada345641.
Tharion, William J., Victoria Goetz, and Miyo Yokota. Estimated Metabolic Heat Production of Helicopter Aircrew Members during Operations in Iraq and Afghanistan. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada558580.
Heaps, Cristine L., and Stefan H. Constable. The Metabolic and Thermoregulatory Responses of Rhesus Monkeys to Combined Exercise and Environmental Heat Load. Fort Belvoir, VA: Defense Technical Information Center, August 1993. http://dx.doi.org/10.21236/ada269756.
Miao, Lina, Hua Qu, and Dazhuo Shi. Prognostic value of the level of gut microbe-generated metabolite trimethylamine-N-oxide in patients with heart failure：a meta-analysis and systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0030.
Miao, Lina, Hua Qu, and Dazhuo Shi. Prognostic value of the level of gut microbe-generated metabolite trimethylamine-N-oxide in patients with heart failure: a meta-analysis and systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0047.
Goetz, Victoria, Miyo Yokota, Anthony J. Karis, and William J. Tharion. Energy Expenditure and Metabolic Heat Production Storage Estimates of Tactical Law Enforcement Personnel during Chemical, Biological, Radiological, and Nuclear (CBRN) Training. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada549510.
Being overweight or obese is linked with heart disease even without other metabolic risk factors. National Institute for Health Research, November 2017. http://dx.doi.org/10.3310/signal-000501.
