Reduced acute myocardial ischemia–reperfusion injury in IL-6-deficient mice employing a closed-chest model
Objective and design We examined the role of IL-6 in the temporal development of cardiac ischemia–reperfusion injury employing a closed-chest I/R model. Materials/methods Infarction, local and systemic inflammation, neutrophil infiltration, coagulation and ST elevation/resolution were compared betwe...
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| Veröffentlicht in: | Inflammation research 2016-06, Vol.65 (6), p.489-499 |
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| creator | Jong, Willeke M. C. ten Cate, Hugo Linnenbank, André C. de Boer, Onno J. Reitsma, Pieter H. de Winter, Robbert J. Zuurbier, Coert J. |
| description | Objective and design
We examined the role of IL-6 in the temporal development of cardiac ischemia–reperfusion injury employing a closed-chest I/R model.
Materials/methods
Infarction, local and systemic inflammation, neutrophil infiltration, coagulation and ST elevation/resolution were compared between wild-type (WT) and IL-6-deficient (IL-6
−/−
) mice after 1 h ischemia and 0, ½, 3, and 24 h reperfusion.
Results
IL-6 deficiency reduced infarct size at 3 h reperfusion (28.8 ± 4.5 % WT vs 17.6 ± 2.5 % IL-6
−/−
), which reduction persisted and remained similar at 24 h reperfusion (25.1 ± 3.0 % WT vs 14.6 ± 4.4 % IL-6
−/−
). Serum Amyloid A was reduced at 24 h reperfusion only (57.5 ± 4.9 WT vs 24.8 ± 5.6 ug/ml IL-6
−/−
mice). Cardiac cytokines (IL-6, IL-1β and TNFα) peaked at 3 h reperfusion, but IL-1β and TNFα levels were unaffected by IL-6 deficiency. Significant neutrophil influx was only detected at 24 h reperfusion and was similar for WT and IL-6
−/−
. Tissue factor peaked at 24 h reperfusion, whereas fibrin/fibrinogen peaked at 3 h reperfusion and was completely resolved at 24 h reperfusion; both coagulation factors were unaltered by IL-6 deficiency. Prolonged ST elevation was observed during ischemia that completely resolved for both genotypes at early reperfusion.
Conclusions
The data suggest that, in the absence of major surgical intervention, IL-6 contributes to the development of infarct size in the early phase of reperfusion; this contribution did not depend on neutrophil influx, IL-1β and TNFα, tissue factor and fibrin. |
| doi_str_mv | 10.1007/s00011-016-0931-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4841857</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4032202071</sourcerecordid><originalsourceid>FETCH-LOGICAL-c503t-a585f7ba0bf8300e24c04b69b80a8a03b8967f434f6e5ab5b98ac42d679837ad3</originalsourceid><addsrcrecordid>eNqNkc-KFDEQxoMo7rr6AF4k4MVLtNJJd9IXQRb_LAwIouAtpNPVsxm6O2MyLczNd9g33CexxlmXVRA8VaB-9dWX-hh7KuGlBDCvCgBIKUA2Alolhb7HTqWuQLRgv96nN1RKKKvghD0qZUO0rWz1kJ1UTatqY-CUjZ-wXwL23Idlh3zap-BzH_3IYwmXOEV__eMq4xbzsJSYZh7nzZL3VPjFSjSixyGGiPOOTzEgx2k7pn2c19zzMKaCvSCVQt3U4_iYPRj8WPDJTT1jX969_Xz-Qaw-vr84f7MSoQa1E7629WA6D91A3gErHUB3TdtZ8NaD6mzbmEErPTRY-67uWuuDrvrGtFYZ36sz9vqou126CftA9rIf3TbHyee9Sz66PztzvHTr9N1pq6WtDQm8uBHI6dtC_t1E58Bx9DOmpThpLO2iCKr_QVUrFaiD6vO_0E1a8kyX-EU1DQWkiZJHKuRUSsbh1rcEd4jdHWN3FLs7xO4OM8_ufvh24nfOBFRHoFBrXmO-s_qfqj8BUSW53A</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1783660004</pqid></control><display><type>article</type><title>Reduced acute myocardial ischemia–reperfusion injury in IL-6-deficient mice employing a closed-chest model</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Jong, Willeke M. C. ; ten Cate, Hugo ; Linnenbank, André C. ; de Boer, Onno J. ; Reitsma, Pieter H. ; de Winter, Robbert J. ; Zuurbier, Coert J.</creator><creatorcontrib>Jong, Willeke M. C. ; ten Cate, Hugo ; Linnenbank, André C. ; de Boer, Onno J. ; Reitsma, Pieter H. ; de Winter, Robbert J. ; Zuurbier, Coert J.</creatorcontrib><description>Objective and design
We examined the role of IL-6 in the temporal development of cardiac ischemia–reperfusion injury employing a closed-chest I/R model.
Materials/methods
Infarction, local and systemic inflammation, neutrophil infiltration, coagulation and ST elevation/resolution were compared between wild-type (WT) and IL-6-deficient (IL-6
−/−
) mice after 1 h ischemia and 0, ½, 3, and 24 h reperfusion.
Results
IL-6 deficiency reduced infarct size at 3 h reperfusion (28.8 ± 4.5 % WT vs 17.6 ± 2.5 % IL-6
−/−
), which reduction persisted and remained similar at 24 h reperfusion (25.1 ± 3.0 % WT vs 14.6 ± 4.4 % IL-6
−/−
). Serum Amyloid A was reduced at 24 h reperfusion only (57.5 ± 4.9 WT vs 24.8 ± 5.6 ug/ml IL-6
−/−
mice). Cardiac cytokines (IL-6, IL-1β and TNFα) peaked at 3 h reperfusion, but IL-1β and TNFα levels were unaffected by IL-6 deficiency. Significant neutrophil influx was only detected at 24 h reperfusion and was similar for WT and IL-6
−/−
. Tissue factor peaked at 24 h reperfusion, whereas fibrin/fibrinogen peaked at 3 h reperfusion and was completely resolved at 24 h reperfusion; both coagulation factors were unaltered by IL-6 deficiency. Prolonged ST elevation was observed during ischemia that completely resolved for both genotypes at early reperfusion.
Conclusions
The data suggest that, in the absence of major surgical intervention, IL-6 contributes to the development of infarct size in the early phase of reperfusion; this contribution did not depend on neutrophil influx, IL-1β and TNFα, tissue factor and fibrin.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-016-0931-4</identifier><identifier>PMID: 26935770</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allergology ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Dermatology ; Immunology ; Interleukin-1beta - blood ; Interleukin-6 - blood ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial Reperfusion Injury - blood ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardium - metabolism ; Myocardium - pathology ; Neurology ; Original Research Paper ; Pharmacology/Toxicology ; Rheumatology ; Tumor Necrosis Factor-alpha - blood</subject><ispartof>Inflammation research, 2016-06, Vol.65 (6), p.489-499</ispartof><rights>The Author(s) 2016</rights><rights>Springer International Publishing 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-a585f7ba0bf8300e24c04b69b80a8a03b8967f434f6e5ab5b98ac42d679837ad3</citedby><cites>FETCH-LOGICAL-c503t-a585f7ba0bf8300e24c04b69b80a8a03b8967f434f6e5ab5b98ac42d679837ad3</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/s00011-016-0931-4$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00011-016-0931-4$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26935770$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jong, Willeke M. C.</creatorcontrib><creatorcontrib>ten Cate, Hugo</creatorcontrib><creatorcontrib>Linnenbank, André C.</creatorcontrib><creatorcontrib>de Boer, Onno J.</creatorcontrib><creatorcontrib>Reitsma, Pieter H.</creatorcontrib><creatorcontrib>de Winter, Robbert J.</creatorcontrib><creatorcontrib>Zuurbier, Coert J.</creatorcontrib><title>Reduced acute myocardial ischemia–reperfusion injury in IL-6-deficient mice employing a closed-chest model</title><title>Inflammation research</title><addtitle>Inflamm. Res</addtitle><addtitle>Inflamm Res</addtitle><description>Objective and design
We examined the role of IL-6 in the temporal development of cardiac ischemia–reperfusion injury employing a closed-chest I/R model.
Materials/methods
Infarction, local and systemic inflammation, neutrophil infiltration, coagulation and ST elevation/resolution were compared between wild-type (WT) and IL-6-deficient (IL-6
−/−
) mice after 1 h ischemia and 0, ½, 3, and 24 h reperfusion.
Results
IL-6 deficiency reduced infarct size at 3 h reperfusion (28.8 ± 4.5 % WT vs 17.6 ± 2.5 % IL-6
−/−
), which reduction persisted and remained similar at 24 h reperfusion (25.1 ± 3.0 % WT vs 14.6 ± 4.4 % IL-6
−/−
). Serum Amyloid A was reduced at 24 h reperfusion only (57.5 ± 4.9 WT vs 24.8 ± 5.6 ug/ml IL-6
−/−
mice). Cardiac cytokines (IL-6, IL-1β and TNFα) peaked at 3 h reperfusion, but IL-1β and TNFα levels were unaffected by IL-6 deficiency. Significant neutrophil influx was only detected at 24 h reperfusion and was similar for WT and IL-6
−/−
. Tissue factor peaked at 24 h reperfusion, whereas fibrin/fibrinogen peaked at 3 h reperfusion and was completely resolved at 24 h reperfusion; both coagulation factors were unaltered by IL-6 deficiency. Prolonged ST elevation was observed during ischemia that completely resolved for both genotypes at early reperfusion.
Conclusions
The data suggest that, in the absence of major surgical intervention, IL-6 contributes to the development of infarct size in the early phase of reperfusion; this contribution did not depend on neutrophil influx, IL-1β and TNFα, tissue factor and fibrin.</description><subject>Allergology</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Dermatology</subject><subject>Immunology</subject><subject>Interleukin-1beta - blood</subject><subject>Interleukin-6 - blood</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myocardial Reperfusion Injury - blood</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Neurology</subject><subject>Original Research Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Rheumatology</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkc-KFDEQxoMo7rr6AF4k4MVLtNJJd9IXQRb_LAwIouAtpNPVsxm6O2MyLczNd9g33CexxlmXVRA8VaB-9dWX-hh7KuGlBDCvCgBIKUA2Alolhb7HTqWuQLRgv96nN1RKKKvghD0qZUO0rWz1kJ1UTatqY-CUjZ-wXwL23Idlh3zap-BzH_3IYwmXOEV__eMq4xbzsJSYZh7nzZL3VPjFSjSixyGGiPOOTzEgx2k7pn2c19zzMKaCvSCVQt3U4_iYPRj8WPDJTT1jX969_Xz-Qaw-vr84f7MSoQa1E7629WA6D91A3gErHUB3TdtZ8NaD6mzbmEErPTRY-67uWuuDrvrGtFYZ36sz9vqou126CftA9rIf3TbHyee9Sz66PztzvHTr9N1pq6WtDQm8uBHI6dtC_t1E58Bx9DOmpThpLO2iCKr_QVUrFaiD6vO_0E1a8kyX-EU1DQWkiZJHKuRUSsbh1rcEd4jdHWN3FLs7xO4OM8_ufvh24nfOBFRHoFBrXmO-s_qfqj8BUSW53A</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Jong, Willeke M. C.</creator><creator>ten Cate, Hugo</creator><creator>Linnenbank, André C.</creator><creator>de Boer, Onno J.</creator><creator>Reitsma, Pieter H.</creator><creator>de Winter, Robbert J.</creator><creator>Zuurbier, Coert J.</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</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>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160601</creationdate><title>Reduced acute myocardial ischemia–reperfusion injury in IL-6-deficient mice employing a closed-chest model</title><author>Jong, Willeke M. C. ; ten Cate, Hugo ; Linnenbank, André C. ; de Boer, Onno J. ; Reitsma, Pieter H. ; de Winter, Robbert J. ; Zuurbier, Coert J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-a585f7ba0bf8300e24c04b69b80a8a03b8967f434f6e5ab5b98ac42d679837ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Allergology</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Dermatology</topic><topic>Immunology</topic><topic>Interleukin-1beta - blood</topic><topic>Interleukin-6 - blood</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myocardial Reperfusion Injury - blood</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Neurology</topic><topic>Original Research Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Rheumatology</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jong, Willeke M. C.</creatorcontrib><creatorcontrib>ten Cate, Hugo</creatorcontrib><creatorcontrib>Linnenbank, André C.</creatorcontrib><creatorcontrib>de Boer, Onno J.</creatorcontrib><creatorcontrib>Reitsma, Pieter H.</creatorcontrib><creatorcontrib>de Winter, Robbert J.</creatorcontrib><creatorcontrib>Zuurbier, Coert J.</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</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>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jong, Willeke M. C.</au><au>ten Cate, Hugo</au><au>Linnenbank, André C.</au><au>de Boer, Onno J.</au><au>Reitsma, Pieter H.</au><au>de Winter, Robbert J.</au><au>Zuurbier, Coert J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced acute myocardial ischemia–reperfusion injury in IL-6-deficient mice employing a closed-chest model</atitle><jtitle>Inflammation research</jtitle><stitle>Inflamm. Res</stitle><addtitle>Inflamm Res</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>65</volume><issue>6</issue><spage>489</spage><epage>499</epage><pages>489-499</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Objective and design
We examined the role of IL-6 in the temporal development of cardiac ischemia–reperfusion injury employing a closed-chest I/R model.
Materials/methods
Infarction, local and systemic inflammation, neutrophil infiltration, coagulation and ST elevation/resolution were compared between wild-type (WT) and IL-6-deficient (IL-6
−/−
) mice after 1 h ischemia and 0, ½, 3, and 24 h reperfusion.
Results
IL-6 deficiency reduced infarct size at 3 h reperfusion (28.8 ± 4.5 % WT vs 17.6 ± 2.5 % IL-6
−/−
), which reduction persisted and remained similar at 24 h reperfusion (25.1 ± 3.0 % WT vs 14.6 ± 4.4 % IL-6
−/−
). Serum Amyloid A was reduced at 24 h reperfusion only (57.5 ± 4.9 WT vs 24.8 ± 5.6 ug/ml IL-6
−/−
mice). Cardiac cytokines (IL-6, IL-1β and TNFα) peaked at 3 h reperfusion, but IL-1β and TNFα levels were unaffected by IL-6 deficiency. Significant neutrophil influx was only detected at 24 h reperfusion and was similar for WT and IL-6
−/−
. Tissue factor peaked at 24 h reperfusion, whereas fibrin/fibrinogen peaked at 3 h reperfusion and was completely resolved at 24 h reperfusion; both coagulation factors were unaltered by IL-6 deficiency. Prolonged ST elevation was observed during ischemia that completely resolved for both genotypes at early reperfusion.
Conclusions
The data suggest that, in the absence of major surgical intervention, IL-6 contributes to the development of infarct size in the early phase of reperfusion; this contribution did not depend on neutrophil influx, IL-1β and TNFα, tissue factor and fibrin.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>26935770</pmid><doi>10.1007/s00011-016-0931-4</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Inflammation research, 2016-06, Vol.65 (6), p.489-499 |
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| language | eng |
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| subjects | Allergology Animals Biomedical and Life Sciences Biomedicine Dermatology Immunology Interleukin-1beta - blood Interleukin-6 - blood Interleukin-6 - genetics Interleukin-6 - metabolism Male Mice, Inbred C57BL Mice, Knockout Myocardial Reperfusion Injury - blood Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardium - metabolism Myocardium - pathology Neurology Original Research Paper Pharmacology/Toxicology Rheumatology Tumor Necrosis Factor-alpha - blood |
| title | Reduced acute myocardial ischemia–reperfusion injury in IL-6-deficient mice employing a closed-chest model |
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