Improved energy supply regulation in chronic hypoxic mouse counteracts hypoxia-induced altered cardiac energetics
Hypoxic states of the cardiovacular system are undoubtedly associated with the most frequent diseases of modern time. Therefore, understanding hypoxic resistance encountered after physiological adaptation such as chronic hypoxia, is crucial to better deal with hypoxic insult. In this study, we exami...
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| description | Hypoxic states of the cardiovacular system are undoubtedly associated with the most frequent diseases of modern time. Therefore, understanding hypoxic resistance encountered after physiological adaptation such as chronic hypoxia, is crucial to better deal with hypoxic insult. In this study, we examine the role of energetic modifications induced by chronic hypoxia (CH) in the higher tolerance to oxygen deprivation.
Swiss mice were exposed to a simulated altitude of 5500 m in a barochamber for 21 days. Isolated perfused hearts were used to study the effects of a decreased oxygen concentration in the perfusate on contractile performance (RPP) and phosphocreatine (PCr) concentration (assessed by (31)P-NMR), and to describe the integrated changes in cardiac energetics regulation by using Modular Control Analysis (MoCA). Oxygen reduction induced a concomitant decrease in RPP (-46%) and in [PCr] (-23%) in Control hearts while CH hearts energetics was unchanged. MoCA demonstrated that this adaptation to hypoxia is the direct consequence of the higher responsiveness (elasticity) of ATP production of CH hearts compared with Controls (-1.88+/-0.38 vs -0.89+/-0.41, p |
| doi_str_mv | 10.1371/journal.pone.0009306 |
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Swiss mice were exposed to a simulated altitude of 5500 m in a barochamber for 21 days. Isolated perfused hearts were used to study the effects of a decreased oxygen concentration in the perfusate on contractile performance (RPP) and phosphocreatine (PCr) concentration (assessed by (31)P-NMR), and to describe the integrated changes in cardiac energetics regulation by using Modular Control Analysis (MoCA). Oxygen reduction induced a concomitant decrease in RPP (-46%) and in [PCr] (-23%) in Control hearts while CH hearts energetics was unchanged. MoCA demonstrated that this adaptation to hypoxia is the direct consequence of the higher responsiveness (elasticity) of ATP production of CH hearts compared with Controls (-1.88+/-0.38 vs -0.89+/-0.41, p<0.01) measured under low oxygen perfusion. This higher elasticity induces an improved response of energy supply to cellular energy demand. The result is the conservation of a healthy control pattern of contraction in CH hearts, whereas Control hearts are severely controlled by energy supply.
As suggested by the present study, the mechanisms responsible for this increase in elasticity and the consequent improved ability of CH heart metabolism to respond to oxygen deprivation could participate to limit the damages induced by hypoxia.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0009306</identifier><identifier>PMID: 20174637</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptation ; Animals ; Biochemistry/Theory and Simulation ; Bioenergetics ; Body Weight ; Cardiovascular Disorders ; Cardiovascular Disorders/Heart Failure ; Chronic Disease ; Computational Biology/Systems Biology ; Conservation ; Contraction ; Control ; Deprivation ; Elasticity ; Energy conservation ; Energy demand ; Energy law ; Energy Metabolism - drug effects ; Energy Metabolism - physiology ; Female ; Heart ; Heart - drug effects ; Heart - physiopathology ; Heart diseases ; Heart failure ; Hypotheses ; Hypoxia ; Hypoxia - physiopathology ; In Vitro Techniques ; Ischemia ; Magnetic Resonance Spectroscopy ; Mathematical models ; Metabolism ; Metabolites ; Mice ; Mitochondria, Heart - metabolism ; Muscle contraction ; Musculoskeletal system ; Myocardial Contraction - drug effects ; Myocardium - metabolism ; Myocardium - pathology ; NMR ; Nuclear magnetic resonance ; Organ Size ; Oxygen ; Oxygen - metabolism ; Oxygen - pharmacology ; Perfusion ; Phosphocreatine ; Phosphocreatine - metabolism ; Physiological aspects ; Physiology ; Physiology/Cardiovascular Physiology and Circulation ; Physiology/Integrative Physiology ; Pulmonary hypertension ; Regulation ; Rodents ; Spectrum analysis ; Studies</subject><ispartof>PloS one, 2010-02, Vol.5 (2), p.e9306</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 Calmettes et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Calmettes et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-be4cebb5f0c12af5b72c7fc9c946d44b2bc1bf8d5df941fb3e6066136bd24d3d3</citedby><cites>FETCH-LOGICAL-c691t-be4cebb5f0c12af5b72c7fc9c946d44b2bc1bf8d5df941fb3e6066136bd24d3d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823784/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823784/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20174637$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Schwartz, Arnold</contributor><creatorcontrib>Calmettes, Guillaume</creatorcontrib><creatorcontrib>Deschodt-Arsac, Véronique</creatorcontrib><creatorcontrib>Gouspillou, Gilles</creatorcontrib><creatorcontrib>Miraux, Sylvain</creatorcontrib><creatorcontrib>Muller, Bernard</creatorcontrib><creatorcontrib>Franconi, Jean-Michel</creatorcontrib><creatorcontrib>Thiaudiere, Eric</creatorcontrib><creatorcontrib>Diolez, Philippe</creatorcontrib><title>Improved energy supply regulation in chronic hypoxic mouse counteracts hypoxia-induced altered cardiac energetics</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Hypoxic states of the cardiovacular system are undoubtedly associated with the most frequent diseases of modern time. Therefore, understanding hypoxic resistance encountered after physiological adaptation such as chronic hypoxia, is crucial to better deal with hypoxic insult. In this study, we examine the role of energetic modifications induced by chronic hypoxia (CH) in the higher tolerance to oxygen deprivation.
Swiss mice were exposed to a simulated altitude of 5500 m in a barochamber for 21 days. Isolated perfused hearts were used to study the effects of a decreased oxygen concentration in the perfusate on contractile performance (RPP) and phosphocreatine (PCr) concentration (assessed by (31)P-NMR), and to describe the integrated changes in cardiac energetics regulation by using Modular Control Analysis (MoCA). Oxygen reduction induced a concomitant decrease in RPP (-46%) and in [PCr] (-23%) in Control hearts while CH hearts energetics was unchanged. MoCA demonstrated that this adaptation to hypoxia is the direct consequence of the higher responsiveness (elasticity) of ATP production of CH hearts compared with Controls (-1.88+/-0.38 vs -0.89+/-0.41, p<0.01) measured under low oxygen perfusion. This higher elasticity induces an improved response of energy supply to cellular energy demand. The result is the conservation of a healthy control pattern of contraction in CH hearts, whereas Control hearts are severely controlled by energy supply.
As suggested by the present study, the mechanisms responsible for this increase in elasticity and the consequent improved ability of CH heart metabolism to respond to oxygen deprivation could participate to limit the damages induced by hypoxia.</description><subject>Adaptation</subject><subject>Animals</subject><subject>Biochemistry/Theory and Simulation</subject><subject>Bioenergetics</subject><subject>Body Weight</subject><subject>Cardiovascular Disorders</subject><subject>Cardiovascular Disorders/Heart Failure</subject><subject>Chronic Disease</subject><subject>Computational Biology/Systems Biology</subject><subject>Conservation</subject><subject>Contraction</subject><subject>Control</subject><subject>Deprivation</subject><subject>Elasticity</subject><subject>Energy conservation</subject><subject>Energy demand</subject><subject>Energy law</subject><subject>Energy Metabolism - drug effects</subject><subject>Energy Metabolism - physiology</subject><subject>Female</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Hypotheses</subject><subject>Hypoxia</subject><subject>Hypoxia - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Ischemia</subject><subject>Magnetic Resonance Spectroscopy</subject><subject>Mathematical models</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Muscle contraction</subject><subject>Musculoskeletal system</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Organ Size</subject><subject>Oxygen</subject><subject>Oxygen - metabolism</subject><subject>Oxygen - pharmacology</subject><subject>Perfusion</subject><subject>Phosphocreatine</subject><subject>Phosphocreatine - metabolism</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Physiology/Cardiovascular Physiology and Circulation</subject><subject>Physiology/Integrative Physiology</subject><subject>Pulmonary hypertension</subject><subject>Regulation</subject><subject>Rodents</subject><subject>Spectrum analysis</subject><subject>Studies</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk0tr3DAQx01padK036C0hkJLD7vVa2X7Egihj4VAoK-rkPXwarElR7JD9tt3tuuEdcmh-DBG85v_jEYzWfYaoyWmBf60DWP0sl32wZslQqiiiD_JTnFFyYITRJ8e_Z9kL1LaIrSiJefPsxOCcME4LU6zm3XXx3BrdG68ic0uT2Pft7s8mmZs5eCCz53P1SYG71S-2fXhDmwXxmRyFUY_mCjVkCaPXDivRwVqsgUPWCWjdlId1M3gVHqZPbOyTebVZM-yX18-_7z8tri6_rq-vLhaKF7hYVEbpkxdryxSmEi7qguiCqsqVTGuGatJrXBtS73StmLY1tRwxDmmvNaEaarpWfb2oNu3IYmpW0lgUlZkVSJKgFgfCB3kVvTRdTLuRJBO_D0IsREyQsmtERqkS4KhksoyZKWknFFZ1pSRolTUgtb5lG2sO6OV8UOU7Ux07vFuI5pwK0hJaFEyEPgwCcRwM5o0iM4lZdpWegPdFgWkqlDFCyDf_UM-frmJaiTU77wNkFbtNcUFK2iFGQwDUMtHKPi06ZyCybIOzmcBH2cBwAzmbmjkmJJY__j-_-z17zn7_ojdGJifTQrtuJ_ANAfZAVQxpBSNfegxRmK_GPfdEPvFENNiQNib4_d5CLrfBPoHtnkLfA</recordid><startdate>20100218</startdate><enddate>20100218</enddate><creator>Calmettes, Guillaume</creator><creator>Deschodt-Arsac, Véronique</creator><creator>Gouspillou, Gilles</creator><creator>Miraux, Sylvain</creator><creator>Muller, Bernard</creator><creator>Franconi, Jean-Michel</creator><creator>Thiaudiere, Eric</creator><creator>Diolez, Philippe</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20100218</creationdate><title>Improved energy supply regulation in chronic hypoxic mouse counteracts hypoxia-induced altered cardiac energetics</title><author>Calmettes, Guillaume ; Deschodt-Arsac, Véronique ; Gouspillou, Gilles ; Miraux, Sylvain ; Muller, Bernard ; Franconi, Jean-Michel ; Thiaudiere, Eric ; Diolez, Philippe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-be4cebb5f0c12af5b72c7fc9c946d44b2bc1bf8d5df941fb3e6066136bd24d3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adaptation</topic><topic>Animals</topic><topic>Biochemistry/Theory and Simulation</topic><topic>Bioenergetics</topic><topic>Body Weight</topic><topic>Cardiovascular Disorders</topic><topic>Cardiovascular Disorders/Heart Failure</topic><topic>Chronic Disease</topic><topic>Computational Biology/Systems Biology</topic><topic>Conservation</topic><topic>Contraction</topic><topic>Control</topic><topic>Deprivation</topic><topic>Elasticity</topic><topic>Energy conservation</topic><topic>Energy demand</topic><topic>Energy law</topic><topic>Energy Metabolism - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Calmettes, Guillaume</au><au>Deschodt-Arsac, Véronique</au><au>Gouspillou, Gilles</au><au>Miraux, Sylvain</au><au>Muller, Bernard</au><au>Franconi, Jean-Michel</au><au>Thiaudiere, Eric</au><au>Diolez, Philippe</au><au>Schwartz, Arnold</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Improved energy supply regulation in chronic hypoxic mouse counteracts hypoxia-induced altered cardiac energetics</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2010-02-18</date><risdate>2010</risdate><volume>5</volume><issue>2</issue><spage>e9306</spage><pages>e9306-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Hypoxic states of the cardiovacular system are undoubtedly associated with the most frequent diseases of modern time. Therefore, understanding hypoxic resistance encountered after physiological adaptation such as chronic hypoxia, is crucial to better deal with hypoxic insult. In this study, we examine the role of energetic modifications induced by chronic hypoxia (CH) in the higher tolerance to oxygen deprivation.
Swiss mice were exposed to a simulated altitude of 5500 m in a barochamber for 21 days. Isolated perfused hearts were used to study the effects of a decreased oxygen concentration in the perfusate on contractile performance (RPP) and phosphocreatine (PCr) concentration (assessed by (31)P-NMR), and to describe the integrated changes in cardiac energetics regulation by using Modular Control Analysis (MoCA). Oxygen reduction induced a concomitant decrease in RPP (-46%) and in [PCr] (-23%) in Control hearts while CH hearts energetics was unchanged. MoCA demonstrated that this adaptation to hypoxia is the direct consequence of the higher responsiveness (elasticity) of ATP production of CH hearts compared with Controls (-1.88+/-0.38 vs -0.89+/-0.41, p<0.01) measured under low oxygen perfusion. This higher elasticity induces an improved response of energy supply to cellular energy demand. The result is the conservation of a healthy control pattern of contraction in CH hearts, whereas Control hearts are severely controlled by energy supply.
As suggested by the present study, the mechanisms responsible for this increase in elasticity and the consequent improved ability of CH heart metabolism to respond to oxygen deprivation could participate to limit the damages induced by hypoxia.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20174637</pmid><doi>10.1371/journal.pone.0009306</doi><tpages>e9306</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adaptation Animals Biochemistry/Theory and Simulation Bioenergetics Body Weight Cardiovascular Disorders Cardiovascular Disorders/Heart Failure Chronic Disease Computational Biology/Systems Biology Conservation Contraction Control Deprivation Elasticity Energy conservation Energy demand Energy law Energy Metabolism - drug effects Energy Metabolism - physiology Female Heart Heart - drug effects Heart - physiopathology Heart diseases Heart failure Hypotheses Hypoxia Hypoxia - physiopathology In Vitro Techniques Ischemia Magnetic Resonance Spectroscopy Mathematical models Metabolism Metabolites Mice Mitochondria, Heart - metabolism Muscle contraction Musculoskeletal system Myocardial Contraction - drug effects Myocardium - metabolism Myocardium - pathology NMR Nuclear magnetic resonance Organ Size Oxygen Oxygen - metabolism Oxygen - pharmacology Perfusion Phosphocreatine Phosphocreatine - metabolism Physiological aspects Physiology Physiology/Cardiovascular Physiology and Circulation Physiology/Integrative Physiology Pulmonary hypertension Regulation Rodents Spectrum analysis Studies |
| title | Improved energy supply regulation in chronic hypoxic mouse counteracts hypoxia-induced altered cardiac energetics |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T01%3A12%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Improved%20energy%20supply%20regulation%20in%20chronic%20hypoxic%20mouse%20counteracts%20hypoxia-induced%20altered%20cardiac%20energetics&rft.jtitle=PloS%20one&rft.au=Calmettes,%20Guillaume&rft.date=2010-02-18&rft.volume=5&rft.issue=2&rft.spage=e9306&rft.pages=e9306-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0009306&rft_dat=%3Cgale_plos_%3EA473914538%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1289258032&rft_id=info:pmid/20174637&rft_galeid=A473914538&rft_doaj_id=oai_doaj_org_article_d66182112a9f40faa3643a8b34278c3f&rfr_iscdi=true |