Neutrophil inhibition contributes to cardioprotection by postconditioning
Background Postconditioning (postcon) reduces infarct size, myocardial superoxide (•O2) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon...
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| creator | GRANFELDT, A. JIANG, R. WANG, N.-P. MYKYTENKO, J. ELDAIF, S. DENEVE, J. ZHAO, Z.-Q. GUYTON, R. A. TØNNESEN, E. VINTEN-JOHANSEN, J. |
| description | Background
Postconditioning (postcon) reduces infarct size, myocardial superoxide (•O2) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon is modified by inhibition of PMNs and (2) postcon directly inhibits PMN •O2 generation.
Methods
For hypothesis 1, a deductive approach was used to determine infarct size in vivo with and without PMNs in rats, and for hypothesis 2, blood sampled from the anterior interventricular vein (AIV) in a canine model was used. Protocol 1: anesthetized rats, subjected to 30 min of coronary artery occlusion and 3 h of reperfusion, were randomized to control (n = 13), postcon (n = 13), PMN‐depletion: (n = 9), and postcon in PMN‐depleted rats (n = 9). Protocol 2: blood was sampled at baseline, 2 h and 24 h from the AIV, draining the area at risk (AAR) in anesthetized dogs with 60 min coronary occlusion ± postcon; whole blood was analyzed for •O2 by luminol‐enhanced chemiluminescence.
Results
Postcon and PMN depletion reduced infarct size (42.6 ± 2.1%, P |
| doi_str_mv | 10.1111/j.1399-6576.2011.02577.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_911933540</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>911933540</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5357-6f2f860bebce466df01f4620c2f81506ead1a1140b10954f997d88481b7861c53</originalsourceid><addsrcrecordid>eNqNkE9v0zAYxi0EYl3HV0C5ILgk-LVjxz5wqCYYq8Y4sGlHy3Ec5pLGnZ2I9tvPaUu5ISxZ_vP-ntePH4QywAWk8XFVAJUy56ziBcEABSasqortCzQ7FV6iGcYYcgYVOUPnMa7SkZZSvkZnhACmvKIzdH1rxyH4zaPrMtc_utoNzveZ8f0QXD0ONmaDz4wOjfOb4Adr9vV6l218HBLW7AWu_3mBXrW6i_bNcZ2j-y-f7y6_5jffr64vFze5YZRVOW9JKziubW1syXnTYmhLTrBJ18Awt7oBDVDiGrBkZStl1QhRCqgrwSH1mKP3h77JztNo46DWLhrbdbq3foxKAkhKWYkT-eGfJGCCRUllmnMkDqgJPsZgW7UJbq3DLkFqilyt1JSsmpJVU-RqH7naJunb4ytjvbbNSfgn4wS8OwI6Gt21QffGxb8cI4wSMX3s04H77Tq7-28DarH4Me2SPj_oXRzs9qTX4ZdKNiqmHm6vlBDL5TcBXC3pM83Oq0o</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1020843984</pqid></control><display><type>article</type><title>Neutrophil inhibition contributes to cardioprotection by postconditioning</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>GRANFELDT, A. ; JIANG, R. ; WANG, N.-P. ; MYKYTENKO, J. ; ELDAIF, S. ; DENEVE, J. ; ZHAO, Z.-Q. ; GUYTON, R. A. ; TØNNESEN, E. ; VINTEN-JOHANSEN, J.</creator><creatorcontrib>GRANFELDT, A. ; JIANG, R. ; WANG, N.-P. ; MYKYTENKO, J. ; ELDAIF, S. ; DENEVE, J. ; ZHAO, Z.-Q. ; GUYTON, R. A. ; TØNNESEN, E. ; VINTEN-JOHANSEN, J.</creatorcontrib><description>Background
Postconditioning (postcon) reduces infarct size, myocardial superoxide (•O2) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon is modified by inhibition of PMNs and (2) postcon directly inhibits PMN •O2 generation.
Methods
For hypothesis 1, a deductive approach was used to determine infarct size in vivo with and without PMNs in rats, and for hypothesis 2, blood sampled from the anterior interventricular vein (AIV) in a canine model was used. Protocol 1: anesthetized rats, subjected to 30 min of coronary artery occlusion and 3 h of reperfusion, were randomized to control (n = 13), postcon (n = 13), PMN‐depletion: (n = 9), and postcon in PMN‐depleted rats (n = 9). Protocol 2: blood was sampled at baseline, 2 h and 24 h from the AIV, draining the area at risk (AAR) in anesthetized dogs with 60 min coronary occlusion ± postcon; whole blood was analyzed for •O2 by luminol‐enhanced chemiluminescence.
Results
Postcon and PMN depletion reduced infarct size (42.6 ± 2.1%, P < 0.05 vs. control, and 43.9 ± 3.0%, P < 0.05 vs. control, respectively) vs. control (58.8 ± 0.9%), with no further decrease with postcon in PMN‐depleted rats (37.2 ± 2.9%, P = 0.34 vs. postcon). PMN accumulation in AAR was less in postcon (21.2 ± 0.3%, P < 0.05 vs. control) and PMN‐depleted (9.4 ± 0.3%, P < 0.05 vs. control) vs. control (30.5 ± 1.2%), with a further decrease in the postcon + PMN depletion group (5.4 ± 0.6%, P < 0.05 vs. control). In dogs, •O2 release by PMNs increased at 2 h and 24 h of R, which was reduced to baseline levels by postcon.
Conclusions
These data imply PMN involvement in cardioprotection by postconditioning.</description><identifier>ISSN: 0001-5172</identifier><identifier>EISSN: 1399-6576</identifier><identifier>DOI: 10.1111/j.1399-6576.2011.02577.x</identifier><identifier>PMID: 22103673</identifier><identifier>CODEN: AANEAB</identifier><language>eng</language><publisher>Oxford: Blackwell Publishing Ltd</publisher><subject>Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Blood ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Chemiluminescence ; coronary artery ; Creatine Kinase - blood ; Data processing ; Dogs ; Heart Rate - drug effects ; Heart Rate - physiology ; Immunohistochemistry ; Ischemic Postconditioning - methods ; Leukocytes (neutrophilic) ; Luminescence ; Luminol ; Male ; Medical sciences ; Myocardial Infarction - pathology ; Myocardial Infarction - prevention & control ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - prevention & control ; Myocardium - pathology ; Necrosis ; Neutrophils - drug effects ; Occlusion ; Oxygen Consumption - drug effects ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Superoxide ; Superoxides - metabolism ; Veins</subject><ispartof>Acta anaesthesiologica Scandinavica, 2012-01, Vol.56 (1), p.48-56</ispartof><rights>2011 The Authors Acta Anaesthesiologica Scandinavica © 2011 The Acta Anaesthesiologica Scandinavica Foundation</rights><rights>2015 INIST-CNRS</rights><rights>2011 The Authors Acta Anaesthesiologica Scandinavica © 2011 The Acta Anaesthesiologica Scandinavica Foundation.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5357-6f2f860bebce466df01f4620c2f81506ead1a1140b10954f997d88481b7861c53</citedby><cites>FETCH-LOGICAL-c5357-6f2f860bebce466df01f4620c2f81506ead1a1140b10954f997d88481b7861c53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1399-6576.2011.02577.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1399-6576.2011.02577.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25253285$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22103673$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GRANFELDT, A.</creatorcontrib><creatorcontrib>JIANG, R.</creatorcontrib><creatorcontrib>WANG, N.-P.</creatorcontrib><creatorcontrib>MYKYTENKO, J.</creatorcontrib><creatorcontrib>ELDAIF, S.</creatorcontrib><creatorcontrib>DENEVE, J.</creatorcontrib><creatorcontrib>ZHAO, Z.-Q.</creatorcontrib><creatorcontrib>GUYTON, R. A.</creatorcontrib><creatorcontrib>TØNNESEN, E.</creatorcontrib><creatorcontrib>VINTEN-JOHANSEN, J.</creatorcontrib><title>Neutrophil inhibition contributes to cardioprotection by postconditioning</title><title>Acta anaesthesiologica Scandinavica</title><addtitle>Acta Anaesthesiol Scand</addtitle><description>Background
Postconditioning (postcon) reduces infarct size, myocardial superoxide (•O2) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon is modified by inhibition of PMNs and (2) postcon directly inhibits PMN •O2 generation.
Methods
For hypothesis 1, a deductive approach was used to determine infarct size in vivo with and without PMNs in rats, and for hypothesis 2, blood sampled from the anterior interventricular vein (AIV) in a canine model was used. Protocol 1: anesthetized rats, subjected to 30 min of coronary artery occlusion and 3 h of reperfusion, were randomized to control (n = 13), postcon (n = 13), PMN‐depletion: (n = 9), and postcon in PMN‐depleted rats (n = 9). Protocol 2: blood was sampled at baseline, 2 h and 24 h from the AIV, draining the area at risk (AAR) in anesthetized dogs with 60 min coronary occlusion ± postcon; whole blood was analyzed for •O2 by luminol‐enhanced chemiluminescence.
Results
Postcon and PMN depletion reduced infarct size (42.6 ± 2.1%, P < 0.05 vs. control, and 43.9 ± 3.0%, P < 0.05 vs. control, respectively) vs. control (58.8 ± 0.9%), with no further decrease with postcon in PMN‐depleted rats (37.2 ± 2.9%, P = 0.34 vs. postcon). PMN accumulation in AAR was less in postcon (21.2 ± 0.3%, P < 0.05 vs. control) and PMN‐depleted (9.4 ± 0.3%, P < 0.05 vs. control) vs. control (30.5 ± 1.2%), with a further decrease in the postcon + PMN depletion group (5.4 ± 0.6%, P < 0.05 vs. control). In dogs, •O2 release by PMNs increased at 2 h and 24 h of R, which was reduced to baseline levels by postcon.
Conclusions
These data imply PMN involvement in cardioprotection by postconditioning.</description><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Chemiluminescence</subject><subject>coronary artery</subject><subject>Creatine Kinase - blood</subject><subject>Data processing</subject><subject>Dogs</subject><subject>Heart Rate - drug effects</subject><subject>Heart Rate - physiology</subject><subject>Immunohistochemistry</subject><subject>Ischemic Postconditioning - methods</subject><subject>Leukocytes (neutrophilic)</subject><subject>Luminescence</subject><subject>Luminol</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - prevention & control</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocardium - pathology</subject><subject>Necrosis</subject><subject>Neutrophils - drug effects</subject><subject>Occlusion</subject><subject>Oxygen Consumption - drug effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion</subject><subject>Superoxide</subject><subject>Superoxides - metabolism</subject><subject>Veins</subject><issn>0001-5172</issn><issn>1399-6576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE9v0zAYxi0EYl3HV0C5ILgk-LVjxz5wqCYYq8Y4sGlHy3Ec5pLGnZ2I9tvPaUu5ISxZ_vP-ntePH4QywAWk8XFVAJUy56ziBcEABSasqortCzQ7FV6iGcYYcgYVOUPnMa7SkZZSvkZnhACmvKIzdH1rxyH4zaPrMtc_utoNzveZ8f0QXD0ONmaDz4wOjfOb4Adr9vV6l218HBLW7AWu_3mBXrW6i_bNcZ2j-y-f7y6_5jffr64vFze5YZRVOW9JKziubW1syXnTYmhLTrBJ18Awt7oBDVDiGrBkZStl1QhRCqgrwSH1mKP3h77JztNo46DWLhrbdbq3foxKAkhKWYkT-eGfJGCCRUllmnMkDqgJPsZgW7UJbq3DLkFqilyt1JSsmpJVU-RqH7naJunb4ytjvbbNSfgn4wS8OwI6Gt21QffGxb8cI4wSMX3s04H77Tq7-28DarH4Me2SPj_oXRzs9qTX4ZdKNiqmHm6vlBDL5TcBXC3pM83Oq0o</recordid><startdate>201201</startdate><enddate>201201</enddate><creator>GRANFELDT, A.</creator><creator>JIANG, R.</creator><creator>WANG, N.-P.</creator><creator>MYKYTENKO, J.</creator><creator>ELDAIF, S.</creator><creator>DENEVE, J.</creator><creator>ZHAO, Z.-Q.</creator><creator>GUYTON, R. A.</creator><creator>TØNNESEN, E.</creator><creator>VINTEN-JOHANSEN, J.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>201201</creationdate><title>Neutrophil inhibition contributes to cardioprotection by postconditioning</title><author>GRANFELDT, A. ; JIANG, R. ; WANG, N.-P. ; MYKYTENKO, J. ; ELDAIF, S. ; DENEVE, J. ; ZHAO, Z.-Q. ; GUYTON, R. A. ; TØNNESEN, E. ; VINTEN-JOHANSEN, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5357-6f2f860bebce466df01f4620c2f81506ead1a1140b10954f997d88481b7861c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Chemiluminescence</topic><topic>coronary artery</topic><topic>Creatine Kinase - blood</topic><topic>Data processing</topic><topic>Dogs</topic><topic>Heart Rate - drug effects</topic><topic>Heart Rate - physiology</topic><topic>Immunohistochemistry</topic><topic>Ischemic Postconditioning - methods</topic><topic>Leukocytes (neutrophilic)</topic><topic>Luminescence</topic><topic>Luminol</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - prevention & control</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocardium - pathology</topic><topic>Necrosis</topic><topic>Neutrophils - drug effects</topic><topic>Occlusion</topic><topic>Oxygen Consumption - drug effects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion</topic><topic>Superoxide</topic><topic>Superoxides - metabolism</topic><topic>Veins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GRANFELDT, A.</creatorcontrib><creatorcontrib>JIANG, R.</creatorcontrib><creatorcontrib>WANG, N.-P.</creatorcontrib><creatorcontrib>MYKYTENKO, J.</creatorcontrib><creatorcontrib>ELDAIF, S.</creatorcontrib><creatorcontrib>DENEVE, J.</creatorcontrib><creatorcontrib>ZHAO, Z.-Q.</creatorcontrib><creatorcontrib>GUYTON, R. A.</creatorcontrib><creatorcontrib>TØNNESEN, E.</creatorcontrib><creatorcontrib>VINTEN-JOHANSEN, J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Acta anaesthesiologica Scandinavica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GRANFELDT, A.</au><au>JIANG, R.</au><au>WANG, N.-P.</au><au>MYKYTENKO, J.</au><au>ELDAIF, S.</au><au>DENEVE, J.</au><au>ZHAO, Z.-Q.</au><au>GUYTON, R. A.</au><au>TØNNESEN, E.</au><au>VINTEN-JOHANSEN, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neutrophil inhibition contributes to cardioprotection by postconditioning</atitle><jtitle>Acta anaesthesiologica Scandinavica</jtitle><addtitle>Acta Anaesthesiol Scand</addtitle><date>2012-01</date><risdate>2012</risdate><volume>56</volume><issue>1</issue><spage>48</spage><epage>56</epage><pages>48-56</pages><issn>0001-5172</issn><eissn>1399-6576</eissn><coden>AANEAB</coden><abstract>Background
Postconditioning (postcon) reduces infarct size, myocardial superoxide (•O2) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon is modified by inhibition of PMNs and (2) postcon directly inhibits PMN •O2 generation.
Methods
For hypothesis 1, a deductive approach was used to determine infarct size in vivo with and without PMNs in rats, and for hypothesis 2, blood sampled from the anterior interventricular vein (AIV) in a canine model was used. Protocol 1: anesthetized rats, subjected to 30 min of coronary artery occlusion and 3 h of reperfusion, were randomized to control (n = 13), postcon (n = 13), PMN‐depletion: (n = 9), and postcon in PMN‐depleted rats (n = 9). Protocol 2: blood was sampled at baseline, 2 h and 24 h from the AIV, draining the area at risk (AAR) in anesthetized dogs with 60 min coronary occlusion ± postcon; whole blood was analyzed for •O2 by luminol‐enhanced chemiluminescence.
Results
Postcon and PMN depletion reduced infarct size (42.6 ± 2.1%, P < 0.05 vs. control, and 43.9 ± 3.0%, P < 0.05 vs. control, respectively) vs. control (58.8 ± 0.9%), with no further decrease with postcon in PMN‐depleted rats (37.2 ± 2.9%, P = 0.34 vs. postcon). PMN accumulation in AAR was less in postcon (21.2 ± 0.3%, P < 0.05 vs. control) and PMN‐depleted (9.4 ± 0.3%, P < 0.05 vs. control) vs. control (30.5 ± 1.2%), with a further decrease in the postcon + PMN depletion group (5.4 ± 0.6%, P < 0.05 vs. control). In dogs, •O2 release by PMNs increased at 2 h and 24 h of R, which was reduced to baseline levels by postcon.
Conclusions
These data imply PMN involvement in cardioprotection by postconditioning.</abstract><cop>Oxford</cop><pub>Blackwell Publishing Ltd</pub><pmid>22103673</pmid><doi>10.1111/j.1399-6576.2011.02577.x</doi><tpages>9</tpages></addata></record> |
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| subjects | Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Blood Blood Pressure - drug effects Blood Pressure - physiology Chemiluminescence coronary artery Creatine Kinase - blood Data processing Dogs Heart Rate - drug effects Heart Rate - physiology Immunohistochemistry Ischemic Postconditioning - methods Leukocytes (neutrophilic) Luminescence Luminol Male Medical sciences Myocardial Infarction - pathology Myocardial Infarction - prevention & control Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control Myocardium - pathology Necrosis Neutrophils - drug effects Occlusion Oxygen Consumption - drug effects Rats Rats, Sprague-Dawley Reperfusion Superoxide Superoxides - metabolism Veins |
| title | Neutrophil inhibition contributes to cardioprotection by postconditioning |
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