Complete recovery of the heart following exposure to profound hypothermia
Cold injury has been suggested as a potential limitation to the use of temperatures below 10 degrees to 15 degrees C in clinical myocardial preservation. The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each...
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Veröffentlicht in: | The Journal of thoracic and cardiovascular surgery 1981-03, Vol.81 (3), p.455-458 |
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description | Cold injury has been suggested as a potential limitation to the use of temperatures below 10 degrees to 15 degrees C in clinical myocardial preservation. The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each heart was isolated and stabilized; then initial aortic flow, coronary flow, and heart rate were measured. The heart then was perfused in the Langendorf mode with oxygenated Krebs-Henseleit buffer for 20 minutes at 0.5 degree, 4 degrees, 10 degrees, 15 degrees, or 20 degrees C. After being rewarmed to 37 degrees C, the heart was returned to the working mode for final functional measurements. In a control group, the perfusion was kept at 37 degrees C. Recovery of function in hearts exposed to hypothermic perfusion was not significantly different from that observed in the hearts kept at 37 degrees C. When cold exposure time to 0.5 degree C perfusion was extended to 2 hours, heart function still returned to the same level as that of control hearts maintained at 37 degrees C, and adenosine triphosphate (ATP) and glycogen levels were higher than those in the control group. Thus, under these conditions, cold exposure per se, even for 2 hours at temperatures near 0 degree C, has no deleterious effect upon myocardial function and energy metabolism. |
doi_str_mv | 10.1016/s0022-5223(19)37614-7 |
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The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each heart was isolated and stabilized; then initial aortic flow, coronary flow, and heart rate were measured. The heart then was perfused in the Langendorf mode with oxygenated Krebs-Henseleit buffer for 20 minutes at 0.5 degree, 4 degrees, 10 degrees, 15 degrees, or 20 degrees C. After being rewarmed to 37 degrees C, the heart was returned to the working mode for final functional measurements. In a control group, the perfusion was kept at 37 degrees C. Recovery of function in hearts exposed to hypothermic perfusion was not significantly different from that observed in the hearts kept at 37 degrees C. When cold exposure time to 0.5 degree C perfusion was extended to 2 hours, heart function still returned to the same level as that of control hearts maintained at 37 degrees C, and adenosine triphosphate (ATP) and glycogen levels were higher than those in the control group. Thus, under these conditions, cold exposure per se, even for 2 hours at temperatures near 0 degree C, has no deleterious effect upon myocardial function and energy metabolism.</description><identifier>ISSN: 0022-5223</identifier><identifier>EISSN: 1097-685X</identifier><identifier>DOI: 10.1016/s0022-5223(19)37614-7</identifier><identifier>PMID: 7464207</identifier><language>eng</language><publisher>United States: AATS/WTSA</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Cold Temperature - adverse effects ; Coronary Circulation ; Energy Metabolism ; Glycogen - metabolism ; Heart - physiology ; Heart Rate ; L-Lactate Dehydrogenase - metabolism ; Male ; Myocardium - metabolism ; Organ Preservation ; Rats ; Time Factors</subject><ispartof>The Journal of thoracic and cardiovascular surgery, 1981-03, Vol.81 (3), p.455-458</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c382t-f6ad64601349749993d15615556083699b021494a4519cb1bd4b0cb0e3d839de3</citedby><cites>FETCH-LOGICAL-c382t-f6ad64601349749993d15615556083699b021494a4519cb1bd4b0cb0e3d839de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7464207$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shragge, BW</creatorcontrib><creatorcontrib>Digerness, SB</creatorcontrib><creatorcontrib>Blackstone, EH</creatorcontrib><title>Complete recovery of the heart following exposure to profound hypothermia</title><title>The Journal of thoracic and cardiovascular surgery</title><addtitle>J Thorac Cardiovasc Surg</addtitle><description>Cold injury has been suggested as a potential limitation to the use of temperatures below 10 degrees to 15 degrees C in clinical myocardial preservation. The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each heart was isolated and stabilized; then initial aortic flow, coronary flow, and heart rate were measured. The heart then was perfused in the Langendorf mode with oxygenated Krebs-Henseleit buffer for 20 minutes at 0.5 degree, 4 degrees, 10 degrees, 15 degrees, or 20 degrees C. After being rewarmed to 37 degrees C, the heart was returned to the working mode for final functional measurements. In a control group, the perfusion was kept at 37 degrees C. Recovery of function in hearts exposed to hypothermic perfusion was not significantly different from that observed in the hearts kept at 37 degrees C. When cold exposure time to 0.5 degree C perfusion was extended to 2 hours, heart function still returned to the same level as that of control hearts maintained at 37 degrees C, and adenosine triphosphate (ATP) and glycogen levels were higher than those in the control group. Thus, under these conditions, cold exposure per se, even for 2 hours at temperatures near 0 degree C, has no deleterious effect upon myocardial function and energy metabolism.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Cold Temperature - adverse effects</subject><subject>Coronary Circulation</subject><subject>Energy Metabolism</subject><subject>Glycogen - metabolism</subject><subject>Heart - physiology</subject><subject>Heart Rate</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Male</subject><subject>Myocardium - metabolism</subject><subject>Organ Preservation</subject><subject>Rats</subject><subject>Time Factors</subject><issn>0022-5223</issn><issn>1097-685X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1981</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtLw0AUhQdRaq3-BGFWoovo3Mwrs5TiCwouVHA35HHTRJJOnEnU_ntTW-rqbr5z7uEj5BzYNTBQN4GxOI5kHPNLMFdcKxCRPiBTYEZHKpHvh2S6R47JSQgfjDHNwEzIRAslYqan5Gnu2q7BHqnH3H2hX1NX0r5CWmHqe1q6pnHf9WpJ8adzYfBIe0c770o3rAparTs3wr6t01NyVKZNwLPdnZG3-7vX-WO0eH54mt8uopwncR-VKi2UUAy4MFoYY3gBUoGUUrGEK2MyFoMwIhUSTJ5BVoiM5RlDXiTcFMhn5GLbO474HDD0tq1Djk2TrtANwWopY8WFHEG5BXPvQvBY2s7XberXFpjdKLQvGz9248eCsX8KrR5z57sHQ9ZisU_tnP0PqOpl9V17tKFNm2akwX70eUjAciuk5L9fEnlZ</recordid><startdate>198103</startdate><enddate>198103</enddate><creator>Shragge, BW</creator><creator>Digerness, SB</creator><creator>Blackstone, EH</creator><general>AATS/WTSA</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>198103</creationdate><title>Complete recovery of the heart following exposure to profound hypothermia</title><author>Shragge, BW ; Digerness, SB ; Blackstone, EH</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c382t-f6ad64601349749993d15615556083699b021494a4519cb1bd4b0cb0e3d839de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1981</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Cold Temperature - adverse effects</topic><topic>Coronary Circulation</topic><topic>Energy Metabolism</topic><topic>Glycogen - metabolism</topic><topic>Heart - physiology</topic><topic>Heart Rate</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Male</topic><topic>Myocardium - metabolism</topic><topic>Organ Preservation</topic><topic>Rats</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shragge, BW</creatorcontrib><creatorcontrib>Digerness, SB</creatorcontrib><creatorcontrib>Blackstone, EH</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>The Journal of thoracic and cardiovascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shragge, BW</au><au>Digerness, SB</au><au>Blackstone, EH</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Complete recovery of the heart following exposure to profound hypothermia</atitle><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle><addtitle>J Thorac Cardiovasc Surg</addtitle><date>1981-03</date><risdate>1981</risdate><volume>81</volume><issue>3</issue><spage>455</spage><epage>458</epage><pages>455-458</pages><issn>0022-5223</issn><eissn>1097-685X</eissn><abstract>Cold injury has been suggested as a potential limitation to the use of temperatures below 10 degrees to 15 degrees C in clinical myocardial preservation. The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each heart was isolated and stabilized; then initial aortic flow, coronary flow, and heart rate were measured. The heart then was perfused in the Langendorf mode with oxygenated Krebs-Henseleit buffer for 20 minutes at 0.5 degree, 4 degrees, 10 degrees, 15 degrees, or 20 degrees C. After being rewarmed to 37 degrees C, the heart was returned to the working mode for final functional measurements. In a control group, the perfusion was kept at 37 degrees C. Recovery of function in hearts exposed to hypothermic perfusion was not significantly different from that observed in the hearts kept at 37 degrees C. When cold exposure time to 0.5 degree C perfusion was extended to 2 hours, heart function still returned to the same level as that of control hearts maintained at 37 degrees C, and adenosine triphosphate (ATP) and glycogen levels were higher than those in the control group. Thus, under these conditions, cold exposure per se, even for 2 hours at temperatures near 0 degree C, has no deleterious effect upon myocardial function and energy metabolism.</abstract><cop>United States</cop><pub>AATS/WTSA</pub><pmid>7464207</pmid><doi>10.1016/s0022-5223(19)37614-7</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; ScienceDirect Journals (5 years ago - present); EZB-FREE-00999 freely available EZB journals |
subjects | Adenosine Triphosphate - metabolism Animals Cold Temperature - adverse effects Coronary Circulation Energy Metabolism Glycogen - metabolism Heart - physiology Heart Rate L-Lactate Dehydrogenase - metabolism Male Myocardium - metabolism Organ Preservation Rats Time Factors |
title | Complete recovery of the heart following exposure to profound hypothermia |
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