Influence of Deep Hypothermia on the Tolerance of the Isolated Cardiomyocyte to Ischemia–Reperfusion
The influence of deep hypothermia (4°C) during a substrate-free, hypoxia–reoxygenation treatment was investigated on cardiomyocytes (CM) prepared from newborn rat heart in culture in an in vitro, substrate-free model of ischemia–reperfusion. The transmembranous potentials were recorded with standard...
Gespeichert in:
Veröffentlicht in: | Journal of molecular and cellular cardiology 2001-11, Vol.33 (11), p.1973-1988 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 1988 |
---|---|
container_issue | 11 |
container_start_page | 1973 |
container_title | Journal of molecular and cellular cardiology |
container_volume | 33 |
creator | Bes, Sandrine Roussel, Pascal Laubriet, Aline Vandroux, David Tissier, Cindy Rochette, Luc Athias, Pierre |
description | The influence of deep hypothermia (4°C) during a substrate-free, hypoxia–reoxygenation treatment was investigated on cardiomyocytes (CM) prepared from newborn rat heart in culture in an in vitro, substrate-free model of ischemia–reperfusion. The transmembranous potentials were recorded with standard microelectrodes. The contractions were monitored photometrically. The RNA messenger (mRNA) and protein expression for protein (HSP70) were analysed by RT-PCR (reverse transcriptase-polymerase chain reaction) and Western blotting, respectively. Simultated ischemia (SI) caused a gradual decrease and then a cessation of the spontaneous electromechanical activity. During the reoxygenation, the CM recovered normal function, provided that SI did not exceed 2.5 h. When SI duration was increased up to 4 h, reoxygenation failed to restore the spontaneous electromechanical activity. Conversely, the exposure of the CM to SI together with deep hypothermia decreased the functional alterations observed, and provided a complete electromechanical recovery after 2.5 h as well as after 4 h of SI. Deep hypothermia alone failed to induce HSP70 mRNA and protein production. On the contrary, HSP70 mRNA production increased after 2.5 and 4 h of deep hypothermia followed by 1 h of rewarming, proportionally to the duration of the cooling period. This augmentation in mRNA was associated with a rise in HSP70 protein content. In summary, it appeared that deep hypothermia exerts a strong cytoprotectrive action during SI only, whereas cooling CM before SI has no beneficial effect on subsequent SI. Moreover, these results suggested the persistence of a signaling system and/or transduction in deeply cooled, functionally depressed cells. Finally, CM in culture appeared to be a model of interest for studying heart graft protection against ischemia-reperfusion and contributed to clarifying the molecular and cellular mechanisms of deep hypothermia on myocardium. |
doi_str_mv | 10.1006/jmcc.2001.1461 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72284742</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0022282801914610</els_id><sourcerecordid>72284742</sourcerecordid><originalsourceid>FETCH-LOGICAL-c340t-c663ec4228fe57e8b63a03e41a8e4a9f3b7c626311e399ce58924cc51bea152f3</originalsourceid><addsrcrecordid>eNp1kE1Lw0AQhhdRtFavHiUnb6n7lWRzlPrRQkGQel42m1m6JcnG3UTozf_gP_SXmNCAJ08zzDzzwjwI3RC8IBin9_ta6wXFmCwIT8kJmhGcJ7FIBD9FM4wpjamg4gJdhrDHGOecsXN0QUiGheB0hsy6MVUPjYbImegRoI1Wh9Z1O_C1VZFroqGNtq4CryZoHKyDq1QHZbRUvrSuPjh96CDq3LDROxhOf76-36AFb_pgXXOFzoyqAlxPdY7en5-2y1W8eX1ZLx82sWYcd7FOUwaaUyoMJBmIImUKM-BECeAqN6zIdEpTRgiwPNeQiJxyrRNSgCIJNWyO7o65rXcfPYRO1jZoqCrVgOuDzIZonnE6gIsjqL0LwYORrbe18gdJsBzNytGsHM3K0exwcDsl90UN5R8-qRwAcQRg-O_TgpdB21FsaT3oTpbO_pf9C6y-iVk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>72284742</pqid></control><display><type>article</type><title>Influence of Deep Hypothermia on the Tolerance of the Isolated Cardiomyocyte to Ischemia–Reperfusion</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Bes, Sandrine ; Roussel, Pascal ; Laubriet, Aline ; Vandroux, David ; Tissier, Cindy ; Rochette, Luc ; Athias, Pierre</creator><creatorcontrib>Bes, Sandrine ; Roussel, Pascal ; Laubriet, Aline ; Vandroux, David ; Tissier, Cindy ; Rochette, Luc ; Athias, Pierre</creatorcontrib><description>The influence of deep hypothermia (4°C) during a substrate-free, hypoxia–reoxygenation treatment was investigated on cardiomyocytes (CM) prepared from newborn rat heart in culture in an in vitro, substrate-free model of ischemia–reperfusion. The transmembranous potentials were recorded with standard microelectrodes. The contractions were monitored photometrically. The RNA messenger (mRNA) and protein expression for protein (HSP70) were analysed by RT-PCR (reverse transcriptase-polymerase chain reaction) and Western blotting, respectively. Simultated ischemia (SI) caused a gradual decrease and then a cessation of the spontaneous electromechanical activity. During the reoxygenation, the CM recovered normal function, provided that SI did not exceed 2.5 h. When SI duration was increased up to 4 h, reoxygenation failed to restore the spontaneous electromechanical activity. Conversely, the exposure of the CM to SI together with deep hypothermia decreased the functional alterations observed, and provided a complete electromechanical recovery after 2.5 h as well as after 4 h of SI. Deep hypothermia alone failed to induce HSP70 mRNA and protein production. On the contrary, HSP70 mRNA production increased after 2.5 and 4 h of deep hypothermia followed by 1 h of rewarming, proportionally to the duration of the cooling period. This augmentation in mRNA was associated with a rise in HSP70 protein content. In summary, it appeared that deep hypothermia exerts a strong cytoprotectrive action during SI only, whereas cooling CM before SI has no beneficial effect on subsequent SI. Moreover, these results suggested the persistence of a signaling system and/or transduction in deeply cooled, functionally depressed cells. Finally, CM in culture appeared to be a model of interest for studying heart graft protection against ischemia-reperfusion and contributed to clarifying the molecular and cellular mechanisms of deep hypothermia on myocardium.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1006/jmcc.2001.1461</identifier><identifier>PMID: 11708842</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Blotting, Western ; Cardiomyocytes ; Cells, Cultured ; Cellular contractions ; Cellular culture ; Deep hypothermia ; Electrophysiology ; Heat-Shock Proteins - metabolism ; HSP70 ; HSP70 Heat-Shock Proteins - metabolism ; Hypothermia ; Ischemia - metabolism ; Messenger RNA ; Myocardial Ischemia - prevention & control ; Myocardial Reperfusion Injury - prevention & control ; Myocardium - cytology ; Myocardium - metabolism ; Rat ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; RNA - metabolism ; RNA, Messenger - metabolism ; Simulated ischemia–reperfusion ; Temperature ; Time Factors</subject><ispartof>Journal of molecular and cellular cardiology, 2001-11, Vol.33 (11), p.1973-1988</ispartof><rights>2001 Academic Press</rights><rights>Copyright 2001 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c340t-c663ec4228fe57e8b63a03e41a8e4a9f3b7c626311e399ce58924cc51bea152f3</citedby><cites>FETCH-LOGICAL-c340t-c663ec4228fe57e8b63a03e41a8e4a9f3b7c626311e399ce58924cc51bea152f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022282801914610$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11708842$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bes, Sandrine</creatorcontrib><creatorcontrib>Roussel, Pascal</creatorcontrib><creatorcontrib>Laubriet, Aline</creatorcontrib><creatorcontrib>Vandroux, David</creatorcontrib><creatorcontrib>Tissier, Cindy</creatorcontrib><creatorcontrib>Rochette, Luc</creatorcontrib><creatorcontrib>Athias, Pierre</creatorcontrib><title>Influence of Deep Hypothermia on the Tolerance of the Isolated Cardiomyocyte to Ischemia–Reperfusion</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>The influence of deep hypothermia (4°C) during a substrate-free, hypoxia–reoxygenation treatment was investigated on cardiomyocytes (CM) prepared from newborn rat heart in culture in an in vitro, substrate-free model of ischemia–reperfusion. The transmembranous potentials were recorded with standard microelectrodes. The contractions were monitored photometrically. The RNA messenger (mRNA) and protein expression for protein (HSP70) were analysed by RT-PCR (reverse transcriptase-polymerase chain reaction) and Western blotting, respectively. Simultated ischemia (SI) caused a gradual decrease and then a cessation of the spontaneous electromechanical activity. During the reoxygenation, the CM recovered normal function, provided that SI did not exceed 2.5 h. When SI duration was increased up to 4 h, reoxygenation failed to restore the spontaneous electromechanical activity. Conversely, the exposure of the CM to SI together with deep hypothermia decreased the functional alterations observed, and provided a complete electromechanical recovery after 2.5 h as well as after 4 h of SI. Deep hypothermia alone failed to induce HSP70 mRNA and protein production. On the contrary, HSP70 mRNA production increased after 2.5 and 4 h of deep hypothermia followed by 1 h of rewarming, proportionally to the duration of the cooling period. This augmentation in mRNA was associated with a rise in HSP70 protein content. In summary, it appeared that deep hypothermia exerts a strong cytoprotectrive action during SI only, whereas cooling CM before SI has no beneficial effect on subsequent SI. Moreover, these results suggested the persistence of a signaling system and/or transduction in deeply cooled, functionally depressed cells. Finally, CM in culture appeared to be a model of interest for studying heart graft protection against ischemia-reperfusion and contributed to clarifying the molecular and cellular mechanisms of deep hypothermia on myocardium.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cardiomyocytes</subject><subject>Cells, Cultured</subject><subject>Cellular contractions</subject><subject>Cellular culture</subject><subject>Deep hypothermia</subject><subject>Electrophysiology</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>HSP70</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Hypothermia</subject><subject>Ischemia - metabolism</subject><subject>Messenger RNA</subject><subject>Myocardial Ischemia - prevention & control</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Simulated ischemia–reperfusion</subject><subject>Temperature</subject><subject>Time Factors</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1Lw0AQhhdRtFavHiUnb6n7lWRzlPrRQkGQel42m1m6JcnG3UTozf_gP_SXmNCAJ08zzDzzwjwI3RC8IBin9_ta6wXFmCwIT8kJmhGcJ7FIBD9FM4wpjamg4gJdhrDHGOecsXN0QUiGheB0hsy6MVUPjYbImegRoI1Wh9Z1O_C1VZFroqGNtq4CryZoHKyDq1QHZbRUvrSuPjh96CDq3LDROxhOf76-36AFb_pgXXOFzoyqAlxPdY7en5-2y1W8eX1ZLx82sWYcd7FOUwaaUyoMJBmIImUKM-BECeAqN6zIdEpTRgiwPNeQiJxyrRNSgCIJNWyO7o65rXcfPYRO1jZoqCrVgOuDzIZonnE6gIsjqL0LwYORrbe18gdJsBzNytGsHM3K0exwcDsl90UN5R8-qRwAcQRg-O_TgpdB21FsaT3oTpbO_pf9C6y-iVk</recordid><startdate>20011101</startdate><enddate>20011101</enddate><creator>Bes, Sandrine</creator><creator>Roussel, Pascal</creator><creator>Laubriet, Aline</creator><creator>Vandroux, David</creator><creator>Tissier, Cindy</creator><creator>Rochette, Luc</creator><creator>Athias, Pierre</creator><general>Elsevier Ltd</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>7X8</scope></search><sort><creationdate>20011101</creationdate><title>Influence of Deep Hypothermia on the Tolerance of the Isolated Cardiomyocyte to Ischemia–Reperfusion</title><author>Bes, Sandrine ; Roussel, Pascal ; Laubriet, Aline ; Vandroux, David ; Tissier, Cindy ; Rochette, Luc ; Athias, Pierre</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c340t-c663ec4228fe57e8b63a03e41a8e4a9f3b7c626311e399ce58924cc51bea152f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Blotting, Western</topic><topic>Cardiomyocytes</topic><topic>Cells, Cultured</topic><topic>Cellular contractions</topic><topic>Cellular culture</topic><topic>Deep hypothermia</topic><topic>Electrophysiology</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>HSP70</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Hypothermia</topic><topic>Ischemia - metabolism</topic><topic>Messenger RNA</topic><topic>Myocardial Ischemia - prevention & control</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Simulated ischemia–reperfusion</topic><topic>Temperature</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bes, Sandrine</creatorcontrib><creatorcontrib>Roussel, Pascal</creatorcontrib><creatorcontrib>Laubriet, Aline</creatorcontrib><creatorcontrib>Vandroux, David</creatorcontrib><creatorcontrib>Tissier, Cindy</creatorcontrib><creatorcontrib>Rochette, Luc</creatorcontrib><creatorcontrib>Athias, Pierre</creatorcontrib><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><jtitle>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bes, Sandrine</au><au>Roussel, Pascal</au><au>Laubriet, Aline</au><au>Vandroux, David</au><au>Tissier, Cindy</au><au>Rochette, Luc</au><au>Athias, Pierre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influence of Deep Hypothermia on the Tolerance of the Isolated Cardiomyocyte to Ischemia–Reperfusion</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>2001-11-01</date><risdate>2001</risdate><volume>33</volume><issue>11</issue><spage>1973</spage><epage>1988</epage><pages>1973-1988</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>The influence of deep hypothermia (4°C) during a substrate-free, hypoxia–reoxygenation treatment was investigated on cardiomyocytes (CM) prepared from newborn rat heart in culture in an in vitro, substrate-free model of ischemia–reperfusion. The transmembranous potentials were recorded with standard microelectrodes. The contractions were monitored photometrically. The RNA messenger (mRNA) and protein expression for protein (HSP70) were analysed by RT-PCR (reverse transcriptase-polymerase chain reaction) and Western blotting, respectively. Simultated ischemia (SI) caused a gradual decrease and then a cessation of the spontaneous electromechanical activity. During the reoxygenation, the CM recovered normal function, provided that SI did not exceed 2.5 h. When SI duration was increased up to 4 h, reoxygenation failed to restore the spontaneous electromechanical activity. Conversely, the exposure of the CM to SI together with deep hypothermia decreased the functional alterations observed, and provided a complete electromechanical recovery after 2.5 h as well as after 4 h of SI. Deep hypothermia alone failed to induce HSP70 mRNA and protein production. On the contrary, HSP70 mRNA production increased after 2.5 and 4 h of deep hypothermia followed by 1 h of rewarming, proportionally to the duration of the cooling period. This augmentation in mRNA was associated with a rise in HSP70 protein content. In summary, it appeared that deep hypothermia exerts a strong cytoprotectrive action during SI only, whereas cooling CM before SI has no beneficial effect on subsequent SI. Moreover, these results suggested the persistence of a signaling system and/or transduction in deeply cooled, functionally depressed cells. Finally, CM in culture appeared to be a model of interest for studying heart graft protection against ischemia-reperfusion and contributed to clarifying the molecular and cellular mechanisms of deep hypothermia on myocardium.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>11708842</pmid><doi>10.1006/jmcc.2001.1461</doi><tpages>16</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0022-2828 |
ispartof | Journal of molecular and cellular cardiology, 2001-11, Vol.33 (11), p.1973-1988 |
issn | 0022-2828 1095-8584 |
language | eng |
recordid | cdi_proquest_miscellaneous_72284742 |
source | MEDLINE; Elsevier ScienceDirect Journals |
subjects | Animals Blotting, Western Cardiomyocytes Cells, Cultured Cellular contractions Cellular culture Deep hypothermia Electrophysiology Heat-Shock Proteins - metabolism HSP70 HSP70 Heat-Shock Proteins - metabolism Hypothermia Ischemia - metabolism Messenger RNA Myocardial Ischemia - prevention & control Myocardial Reperfusion Injury - prevention & control Myocardium - cytology Myocardium - metabolism Rat Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA - metabolism RNA, Messenger - metabolism Simulated ischemia–reperfusion Temperature Time Factors |
title | Influence of Deep Hypothermia on the Tolerance of the Isolated Cardiomyocyte to Ischemia–Reperfusion |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-15T02%3A24%3A24IST&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=Influence%20of%20Deep%20Hypothermia%20on%20the%20Tolerance%20of%20the%20Isolated%20Cardiomyocyte%20to%20Ischemia%E2%80%93Reperfusion&rft.jtitle=Journal%20of%20molecular%20and%20cellular%20cardiology&rft.au=Bes,%20Sandrine&rft.date=2001-11-01&rft.volume=33&rft.issue=11&rft.spage=1973&rft.epage=1988&rft.pages=1973-1988&rft.issn=0022-2828&rft.eissn=1095-8584&rft_id=info:doi/10.1006/jmcc.2001.1461&rft_dat=%3Cproquest_cross%3E72284742%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=72284742&rft_id=info:pmid/11708842&rft_els_id=S0022282801914610&rfr_iscdi=true |