Cyclosporine A reduces microvascular obstruction and preserves left ventricular function deterioration following myocardial ischemia and reperfusion
Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected to coronary occlusion for 1 h followed by 3 h...
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| creator | Zalewski, Jaroslaw Claus, Piet Bogaert, Jan Driessche, Nina Vanden Driesen, Ronald B. Galan, Diogo T. Sipido, Karin R. Buszman, Piotr Milewski, Krzysztof Van de Werf, Frans |
| description | Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected to coronary occlusion for 1 h followed by 3 h of reperfusion were assigned to control (
n
= 8), postconditioning (
n
= 9) or cyclosporine A intravenous infusion 10–15 min before the end of ischemia (
n
= 8). Postconditioning was induced by 8 cycles of repeated 30-s balloon inflation and deflation. After 3 h of reperfusion magnetic resonance imaging, triphenyltetrazolium chloride/Evans blue staining and histopathology were performed. Microvascular obstruction (MVO, percentage of gadolinium-hyperenhanced area) was measured early (3 min) and late (12 min) after contrast injection. Infarct size with double staining was smaller in cyclosporine (46.2 ± 3.1 %,
P
= 0.016) and postconditioning pigs (47.6 ± 3.9 %,
P
= 0.008) versus controls (53.8 ± 4.1 %). Late MVO was significantly reduced by cyclosporine (13.9 ± 9.6 %,
P
= 0.047) but not postconditioning (23.6 ± 11.7 %,
P
= 0.66) when compared with controls (32.0 ± 16.9 %). Myocardial blood flow in the late MVO was improved with cyclosporine versus controls (0.30 ± 0.06 vs 0.21 ± 0.03 ml/g/min,
P
= 0.002) and was inversely correlated with late-MVO extent (
R
2
= 0.93,
P
|
| doi_str_mv | 10.1007/s00395-015-0475-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4342514</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1660643785</sourcerecordid><originalsourceid>FETCH-LOGICAL-c540t-ff0b16b437cf00db948a5883c7a7391340ce04f07b25fe5717b93c891aba6a353</originalsourceid><addsrcrecordid>eNp1kc-KFDEQxoMo7jj6AF6kwYuX1kon6aQvwjL4Dxa86Dmk05XZLOnOmHSPzHv4wGa212UVPIQQ6pev6quPkJcU3lIA-S4DsE7UQMvhUtTqEdlQzkRNFbDHZAMMoFa8URfkWc43AJS3LX1KLhohGxCKbsiv3cmGmA8x-QmryyrhsFjM1ehtikeT7RJMqmKf57TY2cepMtNQHRJmTMfCBXRzdcRpTn5F3TKt3IAzJh-TuX25GEL86ad9NZ6iNWnwJlQ-22scvbnVTHjA5JZc6OfkiTMh44u7e0u-f_zwbfe5vvr66cvu8qq2gsNcOwc9bXvOpHUAQ99xZYRSzEojWUcZB4vAHci-EQ6FpLLvmFUdNb1pDRNsS96vuoelH3GwZxsm6EPyo0knHY3Xf1cmf6338ag5440om96SN3cCKf5YMM96LJ4wBDNhXLKmbQttmU-de73-B72JS5qKPU2lVLQtSXaFoitVtp9zQnc_DAV9zlyvmeuSuT5nrlX58-qhi_sff0IuQLMCuZSmPaYHrf-r-htq-ryX</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1778163959</pqid></control><display><type>article</type><title>Cyclosporine A reduces microvascular obstruction and preserves left ventricular function deterioration following myocardial ischemia and reperfusion</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Zalewski, Jaroslaw ; Claus, Piet ; Bogaert, Jan ; Driessche, Nina Vanden ; Driesen, Ronald B. ; Galan, Diogo T. ; Sipido, Karin R. ; Buszman, Piotr ; Milewski, Krzysztof ; Van de Werf, Frans</creator><creatorcontrib>Zalewski, Jaroslaw ; Claus, Piet ; Bogaert, Jan ; Driessche, Nina Vanden ; Driesen, Ronald B. ; Galan, Diogo T. ; Sipido, Karin R. ; Buszman, Piotr ; Milewski, Krzysztof ; Van de Werf, Frans</creatorcontrib><description>Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected to coronary occlusion for 1 h followed by 3 h of reperfusion were assigned to control (
n
= 8), postconditioning (
n
= 9) or cyclosporine A intravenous infusion 10–15 min before the end of ischemia (
n
= 8). Postconditioning was induced by 8 cycles of repeated 30-s balloon inflation and deflation. After 3 h of reperfusion magnetic resonance imaging, triphenyltetrazolium chloride/Evans blue staining and histopathology were performed. Microvascular obstruction (MVO, percentage of gadolinium-hyperenhanced area) was measured early (3 min) and late (12 min) after contrast injection. Infarct size with double staining was smaller in cyclosporine (46.2 ± 3.1 %,
P
= 0.016) and postconditioning pigs (47.6 ± 3.9 %,
P
= 0.008) versus controls (53.8 ± 4.1 %). Late MVO was significantly reduced by cyclosporine (13.9 ± 9.6 %,
P
= 0.047) but not postconditioning (23.6 ± 11.7 %,
P
= 0.66) when compared with controls (32.0 ± 16.9 %). Myocardial blood flow in the late MVO was improved with cyclosporine versus controls (0.30 ± 0.06 vs 0.21 ± 0.03 ml/g/min,
P
= 0.002) and was inversely correlated with late-MVO extent (
R
2
= 0.93,
P
< 0.0001). Deterioration of left ventricular ejection fraction (LVEF) between baseline and 3 h of reperfusion was smaller with cyclosporine (−7.9 ± 2.4 %,
P
= 0.008) but not postconditioning (−12.0 ± 5.5 %,
P
= 0.22) when compared with controls (−16.4 ± 5.5 %). In the three groups, infarct size (
β
= −0.69,
P
< 0.001) and late MVO (
β
= −0.33,
P
= 0.02) were independent predictors of LVEF deterioration following ischemia/reperfusion (
R
2
= 0.73,
P
< 0.001). Despite both cyclosporine A and postconditioning reduce infarct size, only cyclosporine A infusion had a beneficial effect on microvascular damage and was associated with better preserved LV function when compared with controls.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/s00395-015-0475-8</identifier><identifier>PMID: 25720581</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Cardiology ; Cyclosporine - pharmacology ; Disease Models, Animal ; Enzyme Inhibitors - pharmacology ; Female ; Ischemic Postconditioning - methods ; Male ; Medicine ; Medicine & Public Health ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - physiopathology ; Myocardial Reperfusion Injury - prevention & control ; Original Contribution ; Swine</subject><ispartof>Basic research in cardiology, 2015-03, Vol.110 (2), p.18-18, Article 18</ispartof><rights>The Author(s) 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-ff0b16b437cf00db948a5883c7a7391340ce04f07b25fe5717b93c891aba6a353</citedby><cites>FETCH-LOGICAL-c540t-ff0b16b437cf00db948a5883c7a7391340ce04f07b25fe5717b93c891aba6a353</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/s00395-015-0475-8$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00395-015-0475-8$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25720581$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zalewski, Jaroslaw</creatorcontrib><creatorcontrib>Claus, Piet</creatorcontrib><creatorcontrib>Bogaert, Jan</creatorcontrib><creatorcontrib>Driessche, Nina Vanden</creatorcontrib><creatorcontrib>Driesen, Ronald B.</creatorcontrib><creatorcontrib>Galan, Diogo T.</creatorcontrib><creatorcontrib>Sipido, Karin R.</creatorcontrib><creatorcontrib>Buszman, Piotr</creatorcontrib><creatorcontrib>Milewski, Krzysztof</creatorcontrib><creatorcontrib>Van de Werf, Frans</creatorcontrib><title>Cyclosporine A reduces microvascular obstruction and preserves left ventricular function deterioration following myocardial ischemia and reperfusion</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><addtitle>Basic Res Cardiol</addtitle><description>Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected to coronary occlusion for 1 h followed by 3 h of reperfusion were assigned to control (
n
= 8), postconditioning (
n
= 9) or cyclosporine A intravenous infusion 10–15 min before the end of ischemia (
n
= 8). Postconditioning was induced by 8 cycles of repeated 30-s balloon inflation and deflation. After 3 h of reperfusion magnetic resonance imaging, triphenyltetrazolium chloride/Evans blue staining and histopathology were performed. Microvascular obstruction (MVO, percentage of gadolinium-hyperenhanced area) was measured early (3 min) and late (12 min) after contrast injection. Infarct size with double staining was smaller in cyclosporine (46.2 ± 3.1 %,
P
= 0.016) and postconditioning pigs (47.6 ± 3.9 %,
P
= 0.008) versus controls (53.8 ± 4.1 %). Late MVO was significantly reduced by cyclosporine (13.9 ± 9.6 %,
P
= 0.047) but not postconditioning (23.6 ± 11.7 %,
P
= 0.66) when compared with controls (32.0 ± 16.9 %). Myocardial blood flow in the late MVO was improved with cyclosporine versus controls (0.30 ± 0.06 vs 0.21 ± 0.03 ml/g/min,
P
= 0.002) and was inversely correlated with late-MVO extent (
R
2
= 0.93,
P
< 0.0001). Deterioration of left ventricular ejection fraction (LVEF) between baseline and 3 h of reperfusion was smaller with cyclosporine (−7.9 ± 2.4 %,
P
= 0.008) but not postconditioning (−12.0 ± 5.5 %,
P
= 0.22) when compared with controls (−16.4 ± 5.5 %). In the three groups, infarct size (
β
= −0.69,
P
< 0.001) and late MVO (
β
= −0.33,
P
= 0.02) were independent predictors of LVEF deterioration following ischemia/reperfusion (
R
2
= 0.73,
P
< 0.001). Despite both cyclosporine A and postconditioning reduce infarct size, only cyclosporine A infusion had a beneficial effect on microvascular damage and was associated with better preserved LV function when compared with controls.</description><subject>Animals</subject><subject>Cardiology</subject><subject>Cyclosporine - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Ischemic Postconditioning - methods</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Original Contribution</subject><subject>Swine</subject><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kc-KFDEQxoMo7jj6AF6kwYuX1kon6aQvwjL4Dxa86Dmk05XZLOnOmHSPzHv4wGa212UVPIQQ6pev6quPkJcU3lIA-S4DsE7UQMvhUtTqEdlQzkRNFbDHZAMMoFa8URfkWc43AJS3LX1KLhohGxCKbsiv3cmGmA8x-QmryyrhsFjM1ehtikeT7RJMqmKf57TY2cepMtNQHRJmTMfCBXRzdcRpTn5F3TKt3IAzJh-TuX25GEL86ad9NZ6iNWnwJlQ-22scvbnVTHjA5JZc6OfkiTMh44u7e0u-f_zwbfe5vvr66cvu8qq2gsNcOwc9bXvOpHUAQ99xZYRSzEojWUcZB4vAHci-EQ6FpLLvmFUdNb1pDRNsS96vuoelH3GwZxsm6EPyo0knHY3Xf1cmf6338ag5440om96SN3cCKf5YMM96LJ4wBDNhXLKmbQttmU-de73-B72JS5qKPU2lVLQtSXaFoitVtp9zQnc_DAV9zlyvmeuSuT5nrlX58-qhi_sff0IuQLMCuZSmPaYHrf-r-htq-ryX</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>Zalewski, Jaroslaw</creator><creator>Claus, Piet</creator><creator>Bogaert, Jan</creator><creator>Driessche, Nina Vanden</creator><creator>Driesen, Ronald B.</creator><creator>Galan, Diogo T.</creator><creator>Sipido, Karin R.</creator><creator>Buszman, Piotr</creator><creator>Milewski, Krzysztof</creator><creator>Van de Werf, Frans</creator><general>Springer Berlin Heidelberg</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>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>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</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>20150301</creationdate><title>Cyclosporine A reduces microvascular obstruction and preserves left ventricular function deterioration following myocardial ischemia and reperfusion</title><author>Zalewski, Jaroslaw ; Claus, Piet ; Bogaert, Jan ; Driessche, Nina Vanden ; Driesen, Ronald B. ; Galan, Diogo T. ; Sipido, Karin R. ; Buszman, Piotr ; Milewski, Krzysztof ; Van de Werf, Frans</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-ff0b16b437cf00db948a5883c7a7391340ce04f07b25fe5717b93c891aba6a353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Cardiology</topic><topic>Cyclosporine - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Ischemic Postconditioning - methods</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Original Contribution</topic><topic>Swine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zalewski, Jaroslaw</creatorcontrib><creatorcontrib>Claus, Piet</creatorcontrib><creatorcontrib>Bogaert, Jan</creatorcontrib><creatorcontrib>Driessche, Nina Vanden</creatorcontrib><creatorcontrib>Driesen, Ronald B.</creatorcontrib><creatorcontrib>Galan, Diogo T.</creatorcontrib><creatorcontrib>Sipido, Karin R.</creatorcontrib><creatorcontrib>Buszman, Piotr</creatorcontrib><creatorcontrib>Milewski, Krzysztof</creatorcontrib><creatorcontrib>Van de Werf, Frans</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>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>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biochemistry Abstracts 1</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>Basic research in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zalewski, Jaroslaw</au><au>Claus, Piet</au><au>Bogaert, Jan</au><au>Driessche, Nina Vanden</au><au>Driesen, Ronald B.</au><au>Galan, Diogo T.</au><au>Sipido, Karin R.</au><au>Buszman, Piotr</au><au>Milewski, Krzysztof</au><au>Van de Werf, Frans</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclosporine A reduces microvascular obstruction and preserves left ventricular function deterioration following myocardial ischemia and reperfusion</atitle><jtitle>Basic research in cardiology</jtitle><stitle>Basic Res Cardiol</stitle><addtitle>Basic Res Cardiol</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>110</volume><issue>2</issue><spage>18</spage><epage>18</epage><pages>18-18</pages><artnum>18</artnum><issn>0300-8428</issn><eissn>1435-1803</eissn><abstract>Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected to coronary occlusion for 1 h followed by 3 h of reperfusion were assigned to control (
n
= 8), postconditioning (
n
= 9) or cyclosporine A intravenous infusion 10–15 min before the end of ischemia (
n
= 8). Postconditioning was induced by 8 cycles of repeated 30-s balloon inflation and deflation. After 3 h of reperfusion magnetic resonance imaging, triphenyltetrazolium chloride/Evans blue staining and histopathology were performed. Microvascular obstruction (MVO, percentage of gadolinium-hyperenhanced area) was measured early (3 min) and late (12 min) after contrast injection. Infarct size with double staining was smaller in cyclosporine (46.2 ± 3.1 %,
P
= 0.016) and postconditioning pigs (47.6 ± 3.9 %,
P
= 0.008) versus controls (53.8 ± 4.1 %). Late MVO was significantly reduced by cyclosporine (13.9 ± 9.6 %,
P
= 0.047) but not postconditioning (23.6 ± 11.7 %,
P
= 0.66) when compared with controls (32.0 ± 16.9 %). Myocardial blood flow in the late MVO was improved with cyclosporine versus controls (0.30 ± 0.06 vs 0.21 ± 0.03 ml/g/min,
P
= 0.002) and was inversely correlated with late-MVO extent (
R
2
= 0.93,
P
< 0.0001). Deterioration of left ventricular ejection fraction (LVEF) between baseline and 3 h of reperfusion was smaller with cyclosporine (−7.9 ± 2.4 %,
P
= 0.008) but not postconditioning (−12.0 ± 5.5 %,
P
= 0.22) when compared with controls (−16.4 ± 5.5 %). In the three groups, infarct size (
β
= −0.69,
P
< 0.001) and late MVO (
β
= −0.33,
P
= 0.02) were independent predictors of LVEF deterioration following ischemia/reperfusion (
R
2
= 0.73,
P
< 0.001). Despite both cyclosporine A and postconditioning reduce infarct size, only cyclosporine A infusion had a beneficial effect on microvascular damage and was associated with better preserved LV function when compared with controls.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>25720581</pmid><doi>10.1007/s00395-015-0475-8</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-8428 |
| ispartof | Basic research in cardiology, 2015-03, Vol.110 (2), p.18-18, Article 18 |
| issn | 0300-8428 1435-1803 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4342514 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Cardiology Cyclosporine - pharmacology Disease Models, Animal Enzyme Inhibitors - pharmacology Female Ischemic Postconditioning - methods Male Medicine Medicine & Public Health Myocardial Infarction - pathology Myocardial Infarction - physiopathology Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - physiopathology Myocardial Reperfusion Injury - prevention & control Original Contribution Swine |
| title | Cyclosporine A reduces microvascular obstruction and preserves left ventricular function deterioration following myocardial ischemia and reperfusion |
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