Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age
Reports on the effect of age and obesity on myocardial ischaemia/reperfusion (I/R) injury and ischaemic preconditioning are contradictory. The aim of this study was to re-evaluate the effects of age and diet-induced obesity (DIO) on myocardial I/R injury and preconditioning potential. Four groups of...
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description | Reports on the effect of age and obesity on myocardial ischaemia/reperfusion (I/R) injury and ischaemic preconditioning are contradictory. The aim of this study was to re-evaluate the effects of age and diet-induced obesity (DIO) on myocardial I/R injury and preconditioning potential.
Four groups of Wistar male rats were used: age-matched controls (AMC) receiving standard rat chow for (i) 16 weeks and (ii) 16 months respectively; DIO rats receiving a sucrose-supplemented diet for (iii) 16 weeks and (iv) 16 months respectively. The ages of groups (i) and (iii) were 22 weeks ("young") and groups (ii) and (iv) 17 months ("middle-aged") at time of experimentation. Isolated perfused working hearts were subjected to 35 min regional ischaemia/1 h reperfusion. Endpoints were infarct size (tetrazolium staining) and functional recovery. Hearts were preconditioned by 3 × 5 min ischaemia/5 min reperfusion. Results were processed using GraphPad Prism statistical software.
Age did not affect baseline heart function before induction of ischaemia and I/R damage as indicated by infarct size and similar values were obtained in hearts from both age groups. Age also had no effect on functional recovery of hearts during reperfusion after regional ischaemia in AMC rats, but cardiac output during reperfusion was better in hearts from middle-aged than young DIO rats. The diet reduced infarct size in hearts from young rats (% of area at risk: AMC: 32.4 ± 3.6; DIO: 20.7 ± 2.9, p |
doi_str_mv | 10.1186/s12899-017-0030-y |
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Four groups of Wistar male rats were used: age-matched controls (AMC) receiving standard rat chow for (i) 16 weeks and (ii) 16 months respectively; DIO rats receiving a sucrose-supplemented diet for (iii) 16 weeks and (iv) 16 months respectively. The ages of groups (i) and (iii) were 22 weeks ("young") and groups (ii) and (iv) 17 months ("middle-aged") at time of experimentation. Isolated perfused working hearts were subjected to 35 min regional ischaemia/1 h reperfusion. Endpoints were infarct size (tetrazolium staining) and functional recovery. Hearts were preconditioned by 3 × 5 min ischaemia/5 min reperfusion. Results were processed using GraphPad Prism statistical software.
Age did not affect baseline heart function before induction of ischaemia and I/R damage as indicated by infarct size and similar values were obtained in hearts from both age groups. Age also had no effect on functional recovery of hearts during reperfusion after regional ischaemia in AMC rats, but cardiac output during reperfusion was better in hearts from middle-aged than young DIO rats. The diet reduced infarct size in hearts from young rats (% of area at risk: AMC: 32.4 ± 3.6; DIO: 20.7 ± 2.9, p < 0.05), with no differences in hearts from middle-aged rats (AMC: 24.6 ± 4.6; DIO: 28.3 ± 13.5, p = NS). Compared to their respective AMC, diet-induced obesity had no significant effect on functional recovery of hearts from both age groups after exposure to regional ischaemia. When exposed to the more severe stress of global ischaemia, the functional recovery potential of middle-aged DIO rats appeared to be impeded compared to hearts of young DIO rats, while age had no effect on the functional recovery of AMC hearts. Preconditioning reduced infarct size in hearts from young control rats and both middle-aged groups, but not from young DIO rats. Age had a significant effect on functional recovery in preconditioning: it was improved in hearts from young control and DIO rats, but depressed in both middle-aged groups.
The data showed that middle-age and obesity had no effect on baseline myocardial function and did not increase susceptibility to I/R damage upon exposure to regional ischaemia. On the contrary, obesity reduced I/R damage in young rats. Preconditioned aging hearts showed a decreased infarct size, but a reduction in functional recovery.</description><identifier>ISSN: 1472-6793</identifier><identifier>EISSN: 1472-6793</identifier><identifier>DOI: 10.1186/s12899-017-0030-y</identifier><identifier>PMID: 28302152</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Aging ; AMP-activated protein kinase ; Angiogenesis ; Animal models ; Animals ; Cardiac conditioning ; Cardiac muscle ; Cardiovascular diseases ; Cardiovascular system ; Cell death ; Coronary artery ; Cyclosporins ; Disease Models, Animal ; Disease Susceptibility ; Heart diseases ; Hyperphagia ; Insulin resistance ; Ischemic Preconditioning, Myocardial - methods ; Kinases ; Life span ; Male ; Membrane permeability ; Myocardial Infarction - metabolism ; Myocardial Reperfusion Injury - complications ; Myocardial Reperfusion Injury - metabolism ; Myocardium - metabolism ; Obesity ; Obesity - complications ; Obesity - metabolism ; pH effects ; Protein kinase ; Rats, Wistar ; Recovery of function ; Rodents ; Signal transduction ; Temperature effects ; Tumors ; Vascular endothelial growth factor</subject><ispartof>BMC physiology, 2017-03, Vol.17 (1), p.3-3, Article 3</ispartof><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342y-d52f403d127430ffabf06807b1ba1853e51167beed3c2cd01a7543d5d07f24de3</citedby><cites>FETCH-LOGICAL-c342y-d52f403d127430ffabf06807b1ba1853e51167beed3c2cd01a7543d5d07f24de3</cites><orcidid>0000-0002-6847-5091</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356245/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356245/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28302152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Webster, I</creatorcontrib><creatorcontrib>Salie, R</creatorcontrib><creatorcontrib>Marais, E</creatorcontrib><creatorcontrib>Fan, W-J</creatorcontrib><creatorcontrib>Maarman, G</creatorcontrib><creatorcontrib>Huisamen, B</creatorcontrib><creatorcontrib>Lochner, A</creatorcontrib><title>Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age</title><title>BMC physiology</title><addtitle>BMC Physiol</addtitle><description>Reports on the effect of age and obesity on myocardial ischaemia/reperfusion (I/R) injury and ischaemic preconditioning are contradictory. The aim of this study was to re-evaluate the effects of age and diet-induced obesity (DIO) on myocardial I/R injury and preconditioning potential.
Four groups of Wistar male rats were used: age-matched controls (AMC) receiving standard rat chow for (i) 16 weeks and (ii) 16 months respectively; DIO rats receiving a sucrose-supplemented diet for (iii) 16 weeks and (iv) 16 months respectively. The ages of groups (i) and (iii) were 22 weeks ("young") and groups (ii) and (iv) 17 months ("middle-aged") at time of experimentation. Isolated perfused working hearts were subjected to 35 min regional ischaemia/1 h reperfusion. Endpoints were infarct size (tetrazolium staining) and functional recovery. Hearts were preconditioned by 3 × 5 min ischaemia/5 min reperfusion. Results were processed using GraphPad Prism statistical software.
Age did not affect baseline heart function before induction of ischaemia and I/R damage as indicated by infarct size and similar values were obtained in hearts from both age groups. Age also had no effect on functional recovery of hearts during reperfusion after regional ischaemia in AMC rats, but cardiac output during reperfusion was better in hearts from middle-aged than young DIO rats. The diet reduced infarct size in hearts from young rats (% of area at risk: AMC: 32.4 ± 3.6; DIO: 20.7 ± 2.9, p < 0.05), with no differences in hearts from middle-aged rats (AMC: 24.6 ± 4.6; DIO: 28.3 ± 13.5, p = NS). Compared to their respective AMC, diet-induced obesity had no significant effect on functional recovery of hearts from both age groups after exposure to regional ischaemia. When exposed to the more severe stress of global ischaemia, the functional recovery potential of middle-aged DIO rats appeared to be impeded compared to hearts of young DIO rats, while age had no effect on the functional recovery of AMC hearts. Preconditioning reduced infarct size in hearts from young control rats and both middle-aged groups, but not from young DIO rats. Age had a significant effect on functional recovery in preconditioning: it was improved in hearts from young control and DIO rats, but depressed in both middle-aged groups.
The data showed that middle-age and obesity had no effect on baseline myocardial function and did not increase susceptibility to I/R damage upon exposure to regional ischaemia. On the contrary, obesity reduced I/R damage in young rats. Preconditioned aging hearts showed a decreased infarct size, but a reduction in functional recovery.</description><subject>Aging</subject><subject>AMP-activated protein kinase</subject><subject>Angiogenesis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Cardiac conditioning</subject><subject>Cardiac muscle</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular system</subject><subject>Cell death</subject><subject>Coronary artery</subject><subject>Cyclosporins</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility</subject><subject>Heart diseases</subject><subject>Hyperphagia</subject><subject>Insulin resistance</subject><subject>Ischemic Preconditioning, Myocardial - methods</subject><subject>Kinases</subject><subject>Life span</subject><subject>Male</subject><subject>Membrane permeability</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Reperfusion Injury - complications</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - metabolism</subject><subject>pH effects</subject><subject>Protein kinase</subject><subject>Rats, Wistar</subject><subject>Recovery of function</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Temperature effects</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><issn>1472-6793</issn><issn>1472-6793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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><recordid>eNpdkU1LHTEUhkNpqV_9AW4k0E03U_M5yXUhiLRWsLjRdcgkJ97I3Mk1mRHm3zfDtaKuknCe85JzHoSOKflJqW5PC2V6tWoIVQ0hnDTzJ7RPhWJNq1b885v7Hjoo5ZFUUAv9Fe0xzQmjku0j_3dOzmYfbY_LVBxsx9jFPo4zHhOOxa0tbKI9zbCFHKYS04DjgFMHpTJn2OIMDTzbfrLjUksBj2vAEAK4sSxP-wBH6EuwfYFvL-chuv_96-7yT3Nze3V9eXHTOC7Y3HjJgiDcU6YEJyHYLpBWE9XRzlItOUhKW9UBeO6Y84RaJQX30hMVmPDAD9H5Lnc7dRvwDoYx295sc9zYPJtko3lfGeLaPKRnI7lsmZA14MdLQE5PE5TRbOoKoO_tAGkqhmqlNWOC0Ip-_4A-pikPdbxKLetVsl0C6Y5yOZWSIbx-hhKzODQ7h6aqMYtDM9eek7dTvHb8l8b_AZNKmYo</recordid><startdate>20170317</startdate><enddate>20170317</enddate><creator>Webster, I</creator><creator>Salie, R</creator><creator>Marais, E</creator><creator>Fan, W-J</creator><creator>Maarman, G</creator><creator>Huisamen, B</creator><creator>Lochner, A</creator><general>BioMed Central</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>7TK</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6847-5091</orcidid></search><sort><creationdate>20170317</creationdate><title>Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age</title><author>Webster, I ; Salie, R ; Marais, E ; Fan, W-J ; Maarman, G ; Huisamen, B ; Lochner, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342y-d52f403d127430ffabf06807b1ba1853e51167beed3c2cd01a7543d5d07f24de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aging</topic><topic>AMP-activated protein kinase</topic><topic>Angiogenesis</topic><topic>Animal models</topic><topic>Animals</topic><topic>Cardiac conditioning</topic><topic>Cardiac muscle</topic><topic>Cardiovascular diseases</topic><topic>Cardiovascular system</topic><topic>Cell death</topic><topic>Coronary artery</topic><topic>Cyclosporins</topic><topic>Disease Models, Animal</topic><topic>Disease Susceptibility</topic><topic>Heart diseases</topic><topic>Hyperphagia</topic><topic>Insulin resistance</topic><topic>Ischemic Preconditioning, Myocardial - methods</topic><topic>Kinases</topic><topic>Life span</topic><topic>Male</topic><topic>Membrane permeability</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Reperfusion Injury - complications</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - metabolism</topic><topic>pH effects</topic><topic>Protein kinase</topic><topic>Rats, Wistar</topic><topic>Recovery of function</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Temperature effects</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Webster, I</creatorcontrib><creatorcontrib>Salie, R</creatorcontrib><creatorcontrib>Marais, E</creatorcontrib><creatorcontrib>Fan, W-J</creatorcontrib><creatorcontrib>Maarman, G</creatorcontrib><creatorcontrib>Huisamen, B</creatorcontrib><creatorcontrib>Lochner, A</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>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Webster, I</au><au>Salie, R</au><au>Marais, E</au><au>Fan, W-J</au><au>Maarman, G</au><au>Huisamen, B</au><au>Lochner, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age</atitle><jtitle>BMC physiology</jtitle><addtitle>BMC Physiol</addtitle><date>2017-03-17</date><risdate>2017</risdate><volume>17</volume><issue>1</issue><spage>3</spage><epage>3</epage><pages>3-3</pages><artnum>3</artnum><issn>1472-6793</issn><eissn>1472-6793</eissn><abstract>Reports on the effect of age and obesity on myocardial ischaemia/reperfusion (I/R) injury and ischaemic preconditioning are contradictory. The aim of this study was to re-evaluate the effects of age and diet-induced obesity (DIO) on myocardial I/R injury and preconditioning potential.
Four groups of Wistar male rats were used: age-matched controls (AMC) receiving standard rat chow for (i) 16 weeks and (ii) 16 months respectively; DIO rats receiving a sucrose-supplemented diet for (iii) 16 weeks and (iv) 16 months respectively. The ages of groups (i) and (iii) were 22 weeks ("young") and groups (ii) and (iv) 17 months ("middle-aged") at time of experimentation. Isolated perfused working hearts were subjected to 35 min regional ischaemia/1 h reperfusion. Endpoints were infarct size (tetrazolium staining) and functional recovery. Hearts were preconditioned by 3 × 5 min ischaemia/5 min reperfusion. Results were processed using GraphPad Prism statistical software.
Age did not affect baseline heart function before induction of ischaemia and I/R damage as indicated by infarct size and similar values were obtained in hearts from both age groups. Age also had no effect on functional recovery of hearts during reperfusion after regional ischaemia in AMC rats, but cardiac output during reperfusion was better in hearts from middle-aged than young DIO rats. The diet reduced infarct size in hearts from young rats (% of area at risk: AMC: 32.4 ± 3.6; DIO: 20.7 ± 2.9, p < 0.05), with no differences in hearts from middle-aged rats (AMC: 24.6 ± 4.6; DIO: 28.3 ± 13.5, p = NS). Compared to their respective AMC, diet-induced obesity had no significant effect on functional recovery of hearts from both age groups after exposure to regional ischaemia. When exposed to the more severe stress of global ischaemia, the functional recovery potential of middle-aged DIO rats appeared to be impeded compared to hearts of young DIO rats, while age had no effect on the functional recovery of AMC hearts. Preconditioning reduced infarct size in hearts from young control rats and both middle-aged groups, but not from young DIO rats. Age had a significant effect on functional recovery in preconditioning: it was improved in hearts from young control and DIO rats, but depressed in both middle-aged groups.
The data showed that middle-age and obesity had no effect on baseline myocardial function and did not increase susceptibility to I/R damage upon exposure to regional ischaemia. On the contrary, obesity reduced I/R damage in young rats. Preconditioned aging hearts showed a decreased infarct size, but a reduction in functional recovery.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>28302152</pmid><doi>10.1186/s12899-017-0030-y</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-6847-5091</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Aging AMP-activated protein kinase Angiogenesis Animal models Animals Cardiac conditioning Cardiac muscle Cardiovascular diseases Cardiovascular system Cell death Coronary artery Cyclosporins Disease Models, Animal Disease Susceptibility Heart diseases Hyperphagia Insulin resistance Ischemic Preconditioning, Myocardial - methods Kinases Life span Male Membrane permeability Myocardial Infarction - metabolism Myocardial Reperfusion Injury - complications Myocardial Reperfusion Injury - metabolism Myocardium - metabolism Obesity Obesity - complications Obesity - metabolism pH effects Protein kinase Rats, Wistar Recovery of function Rodents Signal transduction Temperature effects Tumors Vascular endothelial growth factor |
title | Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age |
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