Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism
Cardiovascular depression due to endotoxemia remains a major cause of mortality in intensive care patients. To determine whether drug-induced alterations in cardiac metabolism may be a viable strategy to reduce endotoxemia-mediated cardiac dysfunction, we assessed endotoxemia-induced changes in gluc...
Gespeichert in:
| Veröffentlicht in: | Basic research in cardiology 2016-03, Vol.111 (2), p.24, Article 24 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 2 |
| container_start_page | 24 |
| container_title | Basic research in cardiology |
| container_volume | 111 |
| creator | Soraya, Hamid Masoud, Waleed G. T. Gandhi, Manoj Garjani, Alireza Clanachan, Alexander S. |
| description | Cardiovascular depression due to endotoxemia remains a major cause of mortality in intensive care patients. To determine whether drug-induced alterations in cardiac metabolism may be a viable strategy to reduce endotoxemia-mediated cardiac dysfunction, we assessed endotoxemia-induced changes in glucose and fatty acid metabolism under aerobic and post-ischemic conditions. Endotoxemia was induced in male Sprague–Dawley rats by lipopolysaccharide (
Escherichia coli
0111:B4c, 4 mg/kg, i.p.) 6 h prior to heart removal for ex vivo assessment of left ventricular (LV) work and rates of glucose metabolism (glucose uptake, glycogen synthesis, glycolysis and glucose oxidation) and palmitate oxidation. Under aerobic conditions, endotoxemic hearts had impaired LV function as judged by echocardiography in vivo (% ejection fraction, 66.0 ± 3.2 vs 78.0 ± 2.1,
p
|
| doi_str_mv | 10.1007/s00395-016-0544-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1771054984</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3973465731</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-baf2c54aba3c7656a9ef21922621b68f42d1cd10a3b2952382b107ff483bc5f73</originalsourceid><addsrcrecordid>eNp1kE1LxDAQhoMo7rr6A7xIwXM1k6Rp600Wv2DFi55Dkia1S9usSYvuvzdlV_HiaQbmfZ-BB6FzwFeAcX4dMKZllmLgKc4YS_MDNAdGsxQKTA_RHFOM04KRYoZOQlhjDIxzOEYzwkvCKYM5qp-3TktfNbJNOqPfZd_ouFbbYMdeD43rE-va1n02fZ2YvnKD-zJdI28S71qTOJtMndqEpOnj3fh6m4RRhcHLwUTiIJVrm9CdoiMr22DO9nOB3u7vXpeP6erl4Wl5u0o1zcmQKmmJzphUkuqcZ1yWxhIoCeEEFC8sIxXoCrCkipQZoQVRgHNrWUGVzmxOF-hyx9149zGaMIi1G30fXwrIc4iayoLFFOxS2rsQvLFi45tO-q0ALCa1YqdWRLViUism8sWePKrOVL-NH5cxQHaBEE9Rif_z-l_qNwb8hWc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1771054984</pqid></control><display><type>article</type><title>Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Soraya, Hamid ; Masoud, Waleed G. T. ; Gandhi, Manoj ; Garjani, Alireza ; Clanachan, Alexander S.</creator><creatorcontrib>Soraya, Hamid ; Masoud, Waleed G. T. ; Gandhi, Manoj ; Garjani, Alireza ; Clanachan, Alexander S.</creatorcontrib><description>Cardiovascular depression due to endotoxemia remains a major cause of mortality in intensive care patients. To determine whether drug-induced alterations in cardiac metabolism may be a viable strategy to reduce endotoxemia-mediated cardiac dysfunction, we assessed endotoxemia-induced changes in glucose and fatty acid metabolism under aerobic and post-ischemic conditions. Endotoxemia was induced in male Sprague–Dawley rats by lipopolysaccharide (
Escherichia coli
0111:B4c, 4 mg/kg, i.p.) 6 h prior to heart removal for ex vivo assessment of left ventricular (LV) work and rates of glucose metabolism (glucose uptake, glycogen synthesis, glycolysis and glucose oxidation) and palmitate oxidation. Under aerobic conditions, endotoxemic hearts had impaired LV function as judged by echocardiography in vivo (% ejection fraction, 66.0 ± 3.2 vs 78.0 ± 2.1,
p
< 0.05) or by LV work ex vivo (2.14 ± 0.16 vs 3.28 ± 0.16, Joules min
−1
g dry wt
−1
,
p
< 0.05). However, rates of glucose uptake, glycogen synthesis, glycolysis, and glucose oxidation were not altered. Palmitate oxidation was lower in endotoxemic hearts in proportion to the decreased workload, thus metabolic efficiency was unaffected. In hearts reperfused following global ischemia, untreated hearts had impaired recovery of LV work (52.3 ± 9.4 %) whereas endotoxemic hearts had significantly higher recovery (105.6 ± 11.3 %,
p
< 0.05). During reperfusion, fatty acid oxidation, acetyl CoA production and metabolic efficiency were similar in both groups. As impaired cardiac function appeared unrelated to depression of energy substrate oxidation, it is unlikely that drug-induced acceleration of fatty acid oxidation will improve mechanical function. The beneficial repartitioning of glucose metabolism in reperfused endotoxemic hearts may contribute to the cardioprotected phenotype.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/s00395-016-0544-7</identifier><identifier>PMID: 26926341</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Carbohydrate Metabolism ; Cardiology ; Echocardiography ; Endotoxemia - diagnostic imaging ; Endotoxemia - metabolism ; Endotoxemia - physiopathology ; Glucose - metabolism ; Heart - physiology ; In Vitro Techniques ; Lipid Metabolism ; Lung - enzymology ; Male ; Medicine ; Medicine & Public Health ; Myocardial Contraction ; Myocardium - metabolism ; Nitric Oxide Synthase - metabolism ; Original Contribution ; Palmitates - metabolism ; Perfusion ; Rats, Sprague-Dawley ; Ventricular Function, Left</subject><ispartof>Basic research in cardiology, 2016-03, Vol.111 (2), p.24, Article 24</ispartof><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-baf2c54aba3c7656a9ef21922621b68f42d1cd10a3b2952382b107ff483bc5f73</citedby><cites>FETCH-LOGICAL-c372t-baf2c54aba3c7656a9ef21922621b68f42d1cd10a3b2952382b107ff483bc5f73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00395-016-0544-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00395-016-0544-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26926341$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Soraya, Hamid</creatorcontrib><creatorcontrib>Masoud, Waleed G. T.</creatorcontrib><creatorcontrib>Gandhi, Manoj</creatorcontrib><creatorcontrib>Garjani, Alireza</creatorcontrib><creatorcontrib>Clanachan, Alexander S.</creatorcontrib><title>Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><addtitle>Basic Res Cardiol</addtitle><description>Cardiovascular depression due to endotoxemia remains a major cause of mortality in intensive care patients. To determine whether drug-induced alterations in cardiac metabolism may be a viable strategy to reduce endotoxemia-mediated cardiac dysfunction, we assessed endotoxemia-induced changes in glucose and fatty acid metabolism under aerobic and post-ischemic conditions. Endotoxemia was induced in male Sprague–Dawley rats by lipopolysaccharide (
Escherichia coli
0111:B4c, 4 mg/kg, i.p.) 6 h prior to heart removal for ex vivo assessment of left ventricular (LV) work and rates of glucose metabolism (glucose uptake, glycogen synthesis, glycolysis and glucose oxidation) and palmitate oxidation. Under aerobic conditions, endotoxemic hearts had impaired LV function as judged by echocardiography in vivo (% ejection fraction, 66.0 ± 3.2 vs 78.0 ± 2.1,
p
< 0.05) or by LV work ex vivo (2.14 ± 0.16 vs 3.28 ± 0.16, Joules min
−1
g dry wt
−1
,
p
< 0.05). However, rates of glucose uptake, glycogen synthesis, glycolysis, and glucose oxidation were not altered. Palmitate oxidation was lower in endotoxemic hearts in proportion to the decreased workload, thus metabolic efficiency was unaffected. In hearts reperfused following global ischemia, untreated hearts had impaired recovery of LV work (52.3 ± 9.4 %) whereas endotoxemic hearts had significantly higher recovery (105.6 ± 11.3 %,
p
< 0.05). During reperfusion, fatty acid oxidation, acetyl CoA production and metabolic efficiency were similar in both groups. As impaired cardiac function appeared unrelated to depression of energy substrate oxidation, it is unlikely that drug-induced acceleration of fatty acid oxidation will improve mechanical function. The beneficial repartitioning of glucose metabolism in reperfused endotoxemic hearts may contribute to the cardioprotected phenotype.</description><subject>Animals</subject><subject>Carbohydrate Metabolism</subject><subject>Cardiology</subject><subject>Echocardiography</subject><subject>Endotoxemia - diagnostic imaging</subject><subject>Endotoxemia - metabolism</subject><subject>Endotoxemia - physiopathology</subject><subject>Glucose - metabolism</subject><subject>Heart - physiology</subject><subject>In Vitro Techniques</subject><subject>Lipid Metabolism</subject><subject>Lung - enzymology</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myocardial Contraction</subject><subject>Myocardium - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Original Contribution</subject><subject>Palmitates - metabolism</subject><subject>Perfusion</subject><subject>Rats, Sprague-Dawley</subject><subject>Ventricular Function, Left</subject><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kE1LxDAQhoMo7rr6A7xIwXM1k6Rp600Wv2DFi55Dkia1S9usSYvuvzdlV_HiaQbmfZ-BB6FzwFeAcX4dMKZllmLgKc4YS_MDNAdGsxQKTA_RHFOM04KRYoZOQlhjDIxzOEYzwkvCKYM5qp-3TktfNbJNOqPfZd_ouFbbYMdeD43rE-va1n02fZ2YvnKD-zJdI28S71qTOJtMndqEpOnj3fh6m4RRhcHLwUTiIJVrm9CdoiMr22DO9nOB3u7vXpeP6erl4Wl5u0o1zcmQKmmJzphUkuqcZ1yWxhIoCeEEFC8sIxXoCrCkipQZoQVRgHNrWUGVzmxOF-hyx9149zGaMIi1G30fXwrIc4iayoLFFOxS2rsQvLFi45tO-q0ALCa1YqdWRLViUism8sWePKrOVL-NH5cxQHaBEE9Rif_z-l_qNwb8hWc</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Soraya, Hamid</creator><creator>Masoud, Waleed G. T.</creator><creator>Gandhi, Manoj</creator><creator>Garjani, Alireza</creator><creator>Clanachan, Alexander S.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20160301</creationdate><title>Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism</title><author>Soraya, Hamid ; Masoud, Waleed G. T. ; Gandhi, Manoj ; Garjani, Alireza ; Clanachan, Alexander S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-baf2c54aba3c7656a9ef21922621b68f42d1cd10a3b2952382b107ff483bc5f73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Carbohydrate Metabolism</topic><topic>Cardiology</topic><topic>Echocardiography</topic><topic>Endotoxemia - diagnostic imaging</topic><topic>Endotoxemia - metabolism</topic><topic>Endotoxemia - physiopathology</topic><topic>Glucose - metabolism</topic><topic>Heart - physiology</topic><topic>In Vitro Techniques</topic><topic>Lipid Metabolism</topic><topic>Lung - enzymology</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Myocardial Contraction</topic><topic>Myocardium - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Original Contribution</topic><topic>Palmitates - metabolism</topic><topic>Perfusion</topic><topic>Rats, Sprague-Dawley</topic><topic>Ventricular Function, Left</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Soraya, Hamid</creatorcontrib><creatorcontrib>Masoud, Waleed G. T.</creatorcontrib><creatorcontrib>Gandhi, Manoj</creatorcontrib><creatorcontrib>Garjani, Alireza</creatorcontrib><creatorcontrib>Clanachan, Alexander S.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Basic research in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Soraya, Hamid</au><au>Masoud, Waleed G. T.</au><au>Gandhi, Manoj</au><au>Garjani, Alireza</au><au>Clanachan, Alexander S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism</atitle><jtitle>Basic research in cardiology</jtitle><stitle>Basic Res Cardiol</stitle><addtitle>Basic Res Cardiol</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>111</volume><issue>2</issue><spage>24</spage><pages>24-</pages><artnum>24</artnum><issn>0300-8428</issn><eissn>1435-1803</eissn><abstract>Cardiovascular depression due to endotoxemia remains a major cause of mortality in intensive care patients. To determine whether drug-induced alterations in cardiac metabolism may be a viable strategy to reduce endotoxemia-mediated cardiac dysfunction, we assessed endotoxemia-induced changes in glucose and fatty acid metabolism under aerobic and post-ischemic conditions. Endotoxemia was induced in male Sprague–Dawley rats by lipopolysaccharide (
Escherichia coli
0111:B4c, 4 mg/kg, i.p.) 6 h prior to heart removal for ex vivo assessment of left ventricular (LV) work and rates of glucose metabolism (glucose uptake, glycogen synthesis, glycolysis and glucose oxidation) and palmitate oxidation. Under aerobic conditions, endotoxemic hearts had impaired LV function as judged by echocardiography in vivo (% ejection fraction, 66.0 ± 3.2 vs 78.0 ± 2.1,
p
< 0.05) or by LV work ex vivo (2.14 ± 0.16 vs 3.28 ± 0.16, Joules min
−1
g dry wt
−1
,
p
< 0.05). However, rates of glucose uptake, glycogen synthesis, glycolysis, and glucose oxidation were not altered. Palmitate oxidation was lower in endotoxemic hearts in proportion to the decreased workload, thus metabolic efficiency was unaffected. In hearts reperfused following global ischemia, untreated hearts had impaired recovery of LV work (52.3 ± 9.4 %) whereas endotoxemic hearts had significantly higher recovery (105.6 ± 11.3 %,
p
< 0.05). During reperfusion, fatty acid oxidation, acetyl CoA production and metabolic efficiency were similar in both groups. As impaired cardiac function appeared unrelated to depression of energy substrate oxidation, it is unlikely that drug-induced acceleration of fatty acid oxidation will improve mechanical function. The beneficial repartitioning of glucose metabolism in reperfused endotoxemic hearts may contribute to the cardioprotected phenotype.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26926341</pmid><doi>10.1007/s00395-016-0544-7</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-8428 |
| ispartof | Basic research in cardiology, 2016-03, Vol.111 (2), p.24, Article 24 |
| issn | 0300-8428 1435-1803 |
| language | eng |
| recordid | cdi_proquest_journals_1771054984 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Animals Carbohydrate Metabolism Cardiology Echocardiography Endotoxemia - diagnostic imaging Endotoxemia - metabolism Endotoxemia - physiopathology Glucose - metabolism Heart - physiology In Vitro Techniques Lipid Metabolism Lung - enzymology Male Medicine Medicine & Public Health Myocardial Contraction Myocardium - metabolism Nitric Oxide Synthase - metabolism Original Contribution Palmitates - metabolism Perfusion Rats, Sprague-Dawley Ventricular Function, Left |
| title | Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-21T09%3A22%3A17IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Myocardial%20mechanical%20dysfunction%20following%20endotoxemia:%20role%20of%20changes%20in%20energy%20substrate%20metabolism&rft.jtitle=Basic%20research%20in%20cardiology&rft.au=Soraya,%20Hamid&rft.date=2016-03-01&rft.volume=111&rft.issue=2&rft.spage=24&rft.pages=24-&rft.artnum=24&rft.issn=0300-8428&rft.eissn=1435-1803&rft_id=info:doi/10.1007/s00395-016-0544-7&rft_dat=%3Cproquest_cross%3E3973465731%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1771054984&rft_id=info:pmid/26926341&rfr_iscdi=true |