Temperature preconditioning of isolated rat hearts â a potent cardioprotective mechanism involving a reduction in oxidative stress and inhibition of the mitochondrial permeability transition pore
We investigate whether temperature preconditioning (TP), induced by short-term hypothermic perfusion and rewarming, may protect hearts against ischaemic/reperfusion injury like ischaemic preconditioning ( IP ). Isolated rat hearts were perfused for 40 min, followed by 25 min global ischaemia and 60...
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| Veröffentlicht in: | The Journal of physiology 2007-06, Vol.581 (3), p.1147-1161 |
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| creator | Khaliulin, Igor Clarke, Samantha J. Lin, Hua Parker, Joanna Suleiman, M.‐Saadeh Halestrap, Andrew P. |
| description | We investigate whether temperature preconditioning (TP), induced by short-term hypothermic perfusion and rewarming, may protect
hearts against ischaemic/reperfusion injury like ischaemic preconditioning ( IP ). Isolated rat hearts were perfused for 40 min, followed by 25 min global ischaemia and 60 min reperfusion (37°C). During
pre-ischaemia, IP hearts underwent three cycles of 2 min global ischaemia and 3 min reperfusion at 37°C, whereas TP hearts
received three cycles of 2 min hypothermic perfusion (26°C) interspersed by 3 min normothermic perfusion. Other hearts received
a single 6 min hypothermic perfusion (SHP) before ischaemia. Both IP and TP protocols increased levels of high energy phosphates
in the pre-ischaemic heart. During reperfusion, TP improved haemodynamic recovery, decreased arrhythmias and reduced necrotic
damage (lactate dehydrogenase release) more than IP or SHP. Measurements of tissue NAD + levels and calcium-induced swelling of mitochondria isolated at 3 min reperfusion were consistent with greater inhibition
of the mitochondrial permeability transition at reperfusion by TP than IP; this correlated with decreased protein carbonylation,
a surrogate marker for oxidative stress. TP increased protein kinase Cε (PKCε) translocation to the particulate fraction and
pretreatment with chelerythrine (PKC inhibitor) blocked the protective effect of TP. TP also increased phosphorylation of
AMP-activated protein kinase (AMPK) after 5 min index ischaemia, but not before ischaemia. Compound C (AMPK inhibitor) partially
blocked cardioprotection by TP, suggesting that both PKC and AMPK may mediate the effects of TP. The presence of N -(2-mercaptopropionyl) glycine during TP also abolished cardioprotection, indicating an involvement of free radicals in the
signalling mechanism. |
| doi_str_mv | 10.1113/jphysiol.2007.130369 |
| format | Article |
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hearts against ischaemic/reperfusion injury like ischaemic preconditioning ( IP ). Isolated rat hearts were perfused for 40 min, followed by 25 min global ischaemia and 60 min reperfusion (37°C). During
pre-ischaemia, IP hearts underwent three cycles of 2 min global ischaemia and 3 min reperfusion at 37°C, whereas TP hearts
received three cycles of 2 min hypothermic perfusion (26°C) interspersed by 3 min normothermic perfusion. Other hearts received
a single 6 min hypothermic perfusion (SHP) before ischaemia. Both IP and TP protocols increased levels of high energy phosphates
in the pre-ischaemic heart. During reperfusion, TP improved haemodynamic recovery, decreased arrhythmias and reduced necrotic
damage (lactate dehydrogenase release) more than IP or SHP. Measurements of tissue NAD + levels and calcium-induced swelling of mitochondria isolated at 3 min reperfusion were consistent with greater inhibition
of the mitochondrial permeability transition at reperfusion by TP than IP; this correlated with decreased protein carbonylation,
a surrogate marker for oxidative stress. TP increased protein kinase Cε (PKCε) translocation to the particulate fraction and
pretreatment with chelerythrine (PKC inhibitor) blocked the protective effect of TP. TP also increased phosphorylation of
AMP-activated protein kinase (AMPK) after 5 min index ischaemia, but not before ischaemia. Compound C (AMPK inhibitor) partially
blocked cardioprotection by TP, suggesting that both PKC and AMPK may mediate the effects of TP. The presence of N -(2-mercaptopropionyl) glycine during TP also abolished cardioprotection, indicating an involvement of free radicals in the
signalling mechanism.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2007.130369</identifier><identifier>PMID: 17395631</identifier><language>eng</language><publisher>Oxford, UK: The Physiological Society</publisher><subject>AMP-Activated Protein Kinases ; Animals ; Arrhythmias, Cardiac - etiology ; Arrhythmias, Cardiac - metabolism ; Arrhythmias, Cardiac - prevention & control ; Cardiovascular ; Coronary Circulation ; Hypothermia, Induced ; In Vitro Techniques ; Ischemic Preconditioning, Myocardial ; L-Lactate Dehydrogenase - metabolism ; Male ; Mitochondria, Heart - metabolism ; Mitochondria, Heart - pathology ; Mitochondrial Membrane Transport Proteins - metabolism ; Mitochondrial Permeability Transition Pore ; Mitochondrial Swelling ; Multienzyme Complexes - metabolism ; Myocardial Reperfusion Injury - complications ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - physiopathology ; Myocardial Reperfusion Injury - prevention & control ; Myocardium - metabolism ; Myocardium - pathology ; NAD - metabolism ; Necrosis ; Oxidative Stress ; Perfusion ; Phosphocreatine - metabolism ; Phosphorylation ; Protein Carbonylation ; Protein Kinase C-epsilon - metabolism ; Protein Serine-Threonine Kinases - metabolism ; Protein Transport ; Rats ; Rats, Wistar ; Reactive Oxygen Species - metabolism ; Rewarming ; Signal Transduction ; Temperature</subject><ispartof>The Journal of physiology, 2007-06, Vol.581 (3), p.1147-1161</ispartof><rights>2007 The Journal of Physiology © 2007 The Physiological Society</rights><rights>2007 The Authors. Journal compilation © 2007 The Physiological Society 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4899-d3ed65a2e2416bf225cb6763a9af6aa457257881541e78fcdb91c94af884b0373</citedby><cites>FETCH-LOGICAL-c4899-d3ed65a2e2416bf225cb6763a9af6aa457257881541e78fcdb91c94af884b0373</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/PMC1976396/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1976396/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,729,782,786,887,1419,1435,27933,27934,45583,45584,46418,46842,53800,53802</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17395631$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khaliulin, Igor</creatorcontrib><creatorcontrib>Clarke, Samantha J.</creatorcontrib><creatorcontrib>Lin, Hua</creatorcontrib><creatorcontrib>Parker, Joanna</creatorcontrib><creatorcontrib>Suleiman, M.‐Saadeh</creatorcontrib><creatorcontrib>Halestrap, Andrew P.</creatorcontrib><title>Temperature preconditioning of isolated rat hearts â a potent cardioprotective mechanism involving a reduction in oxidative stress and inhibition of the mitochondrial permeability transition pore</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>We investigate whether temperature preconditioning (TP), induced by short-term hypothermic perfusion and rewarming, may protect
hearts against ischaemic/reperfusion injury like ischaemic preconditioning ( IP ). Isolated rat hearts were perfused for 40 min, followed by 25 min global ischaemia and 60 min reperfusion (37°C). During
pre-ischaemia, IP hearts underwent three cycles of 2 min global ischaemia and 3 min reperfusion at 37°C, whereas TP hearts
received three cycles of 2 min hypothermic perfusion (26°C) interspersed by 3 min normothermic perfusion. Other hearts received
a single 6 min hypothermic perfusion (SHP) before ischaemia. Both IP and TP protocols increased levels of high energy phosphates
in the pre-ischaemic heart. During reperfusion, TP improved haemodynamic recovery, decreased arrhythmias and reduced necrotic
damage (lactate dehydrogenase release) more than IP or SHP. Measurements of tissue NAD + levels and calcium-induced swelling of mitochondria isolated at 3 min reperfusion were consistent with greater inhibition
of the mitochondrial permeability transition at reperfusion by TP than IP; this correlated with decreased protein carbonylation,
a surrogate marker for oxidative stress. TP increased protein kinase Cε (PKCε) translocation to the particulate fraction and
pretreatment with chelerythrine (PKC inhibitor) blocked the protective effect of TP. TP also increased phosphorylation of
AMP-activated protein kinase (AMPK) after 5 min index ischaemia, but not before ischaemia. Compound C (AMPK inhibitor) partially
blocked cardioprotection by TP, suggesting that both PKC and AMPK may mediate the effects of TP. The presence of N -(2-mercaptopropionyl) glycine during TP also abolished cardioprotection, indicating an involvement of free radicals in the
signalling mechanism.</description><subject>AMP-Activated Protein Kinases</subject><subject>Animals</subject><subject>Arrhythmias, Cardiac - etiology</subject><subject>Arrhythmias, Cardiac - metabolism</subject><subject>Arrhythmias, Cardiac - prevention & control</subject><subject>Cardiovascular</subject><subject>Coronary Circulation</subject><subject>Hypothermia, Induced</subject><subject>In Vitro Techniques</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Male</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Mitochondria, Heart - pathology</subject><subject>Mitochondrial Membrane Transport Proteins - metabolism</subject><subject>Mitochondrial Permeability Transition Pore</subject><subject>Mitochondrial Swelling</subject><subject>Multienzyme Complexes - metabolism</subject><subject>Myocardial Reperfusion Injury - complications</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>NAD - metabolism</subject><subject>Necrosis</subject><subject>Oxidative Stress</subject><subject>Perfusion</subject><subject>Phosphocreatine - metabolism</subject><subject>Phosphorylation</subject><subject>Protein Carbonylation</subject><subject>Protein Kinase C-epsilon - metabolism</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Protein Transport</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rewarming</subject><subject>Signal Transduction</subject><subject>Temperature</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNqNkkuO1DAQhiMEYpqBGyDkFWLTjR9JHG-Q0IinRoLFsLYqTqXjURIH290zveMO3ICjDBuOhTNpXjtWlu2vvr9kV5Y9ZnTDGBPPL6fuEKzrN5xSuWGCilLdyVYsL9VaSiXuZitKOV8LWbCT7EEIl5QmSqn72QmTQhWlYKvsxwUOE3qIO49k8mjc2Nho3WjHLXEtscH1ELEhCSEdgo-BfP928-XmKwEyuYhjJAZ8Y93k085Eu0cyoOlgtGEgdty7fj-7gHhsdmZWp1Pirm0Dt3CIHkMgMDbpvLP1bfocHbtkstGZLvXkLfQkNTog1La38UCihzEs8OQ8PszutdAHfHRcT7NPr19dnL1dn3948-7s5fna5JVS60ZgUxbAkeesrFvOC1OXshSgoC0B8kLyQlYVK3KGsmpNUytmVA5tVeU1FVKcZi8W77SrB2xMegAPvZ68HcAftAOr_70Zbae3bq-ZSjGqTIKnR4F3n3cYoh5sMNj3MKLbBS1pySmTNIH5AhrvQvDY_g5hVM8joH-NgJ5HQC8jkMqe_N3gn6LjnydALcCV7fHwX1J98f4j52yWP1tqO7vtrqxHvdDBGYvxoIuKaZE8uRQ_AeNH2ik</recordid><startdate>20070615</startdate><enddate>20070615</enddate><creator>Khaliulin, Igor</creator><creator>Clarke, Samantha J.</creator><creator>Lin, Hua</creator><creator>Parker, Joanna</creator><creator>Suleiman, M.‐Saadeh</creator><creator>Halestrap, Andrew P.</creator><general>The Physiological Society</general><general>Blackwell Publishing Ltd</general><scope>24P</scope><scope>WIN</scope><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20070615</creationdate><title>Temperature preconditioning of isolated rat hearts â a potent cardioprotective mechanism involving a reduction in oxidative stress and inhibition of the mitochondrial permeability transition pore</title><author>Khaliulin, Igor ; Clarke, Samantha J. ; Lin, Hua ; Parker, Joanna ; Suleiman, M.‐Saadeh ; Halestrap, Andrew P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4899-d3ed65a2e2416bf225cb6763a9af6aa457257881541e78fcdb91c94af884b0373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>AMP-Activated Protein Kinases</topic><topic>Animals</topic><topic>Arrhythmias, Cardiac - etiology</topic><topic>Arrhythmias, Cardiac - metabolism</topic><topic>Arrhythmias, Cardiac - prevention & control</topic><topic>Cardiovascular</topic><topic>Coronary Circulation</topic><topic>Hypothermia, Induced</topic><topic>In Vitro Techniques</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Male</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Mitochondria, Heart - pathology</topic><topic>Mitochondrial Membrane Transport Proteins - metabolism</topic><topic>Mitochondrial Permeability Transition Pore</topic><topic>Mitochondrial Swelling</topic><topic>Multienzyme Complexes - metabolism</topic><topic>Myocardial Reperfusion Injury - complications</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>NAD - metabolism</topic><topic>Necrosis</topic><topic>Oxidative Stress</topic><topic>Perfusion</topic><topic>Phosphocreatine - metabolism</topic><topic>Phosphorylation</topic><topic>Protein Carbonylation</topic><topic>Protein Kinase C-epsilon - metabolism</topic><topic>Protein Serine-Threonine Kinases - metabolism</topic><topic>Protein Transport</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rewarming</topic><topic>Signal Transduction</topic><topic>Temperature</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khaliulin, Igor</creatorcontrib><creatorcontrib>Clarke, Samantha J.</creatorcontrib><creatorcontrib>Lin, Hua</creatorcontrib><creatorcontrib>Parker, Joanna</creatorcontrib><creatorcontrib>Suleiman, M.‐Saadeh</creatorcontrib><creatorcontrib>Halestrap, Andrew P.</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khaliulin, Igor</au><au>Clarke, Samantha J.</au><au>Lin, Hua</au><au>Parker, Joanna</au><au>Suleiman, M.‐Saadeh</au><au>Halestrap, Andrew P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Temperature preconditioning of isolated rat hearts â a potent cardioprotective mechanism involving a reduction in oxidative stress and inhibition of the mitochondrial permeability transition pore</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2007-06-15</date><risdate>2007</risdate><volume>581</volume><issue>3</issue><spage>1147</spage><epage>1161</epage><pages>1147-1161</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>We investigate whether temperature preconditioning (TP), induced by short-term hypothermic perfusion and rewarming, may protect
hearts against ischaemic/reperfusion injury like ischaemic preconditioning ( IP ). Isolated rat hearts were perfused for 40 min, followed by 25 min global ischaemia and 60 min reperfusion (37°C). During
pre-ischaemia, IP hearts underwent three cycles of 2 min global ischaemia and 3 min reperfusion at 37°C, whereas TP hearts
received three cycles of 2 min hypothermic perfusion (26°C) interspersed by 3 min normothermic perfusion. Other hearts received
a single 6 min hypothermic perfusion (SHP) before ischaemia. Both IP and TP protocols increased levels of high energy phosphates
in the pre-ischaemic heart. During reperfusion, TP improved haemodynamic recovery, decreased arrhythmias and reduced necrotic
damage (lactate dehydrogenase release) more than IP or SHP. Measurements of tissue NAD + levels and calcium-induced swelling of mitochondria isolated at 3 min reperfusion were consistent with greater inhibition
of the mitochondrial permeability transition at reperfusion by TP than IP; this correlated with decreased protein carbonylation,
a surrogate marker for oxidative stress. TP increased protein kinase Cε (PKCε) translocation to the particulate fraction and
pretreatment with chelerythrine (PKC inhibitor) blocked the protective effect of TP. TP also increased phosphorylation of
AMP-activated protein kinase (AMPK) after 5 min index ischaemia, but not before ischaemia. Compound C (AMPK inhibitor) partially
blocked cardioprotection by TP, suggesting that both PKC and AMPK may mediate the effects of TP. The presence of N -(2-mercaptopropionyl) glycine during TP also abolished cardioprotection, indicating an involvement of free radicals in the
signalling mechanism.</abstract><cop>Oxford, UK</cop><pub>The Physiological Society</pub><pmid>17395631</pmid><doi>10.1113/jphysiol.2007.130369</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 2007-06, Vol.581 (3), p.1147-1161 |
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| source | MEDLINE; Access via Wiley Online Library; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | AMP-Activated Protein Kinases Animals Arrhythmias, Cardiac - etiology Arrhythmias, Cardiac - metabolism Arrhythmias, Cardiac - prevention & control Cardiovascular Coronary Circulation Hypothermia, Induced In Vitro Techniques Ischemic Preconditioning, Myocardial L-Lactate Dehydrogenase - metabolism Male Mitochondria, Heart - metabolism Mitochondria, Heart - pathology Mitochondrial Membrane Transport Proteins - metabolism Mitochondrial Permeability Transition Pore Mitochondrial Swelling Multienzyme Complexes - metabolism Myocardial Reperfusion Injury - complications Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - physiopathology Myocardial Reperfusion Injury - prevention & control Myocardium - metabolism Myocardium - pathology NAD - metabolism Necrosis Oxidative Stress Perfusion Phosphocreatine - metabolism Phosphorylation Protein Carbonylation Protein Kinase C-epsilon - metabolism Protein Serine-Threonine Kinases - metabolism Protein Transport Rats Rats, Wistar Reactive Oxygen Species - metabolism Rewarming Signal Transduction Temperature |
| title | Temperature preconditioning of isolated rat hearts â a potent cardioprotective mechanism involving a reduction in oxidative stress and inhibition of the mitochondrial permeability transition pore |
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