Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium
Background. This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium. Methods. In 20 pigs, the second and third diagonal coronary arteries were occlu...
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| Veröffentlicht in: | The Annals of thoracic surgery 1998-04, Vol.65 (4), p.973-977 |
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| creator | Lazar, Harold L. Hamasaki, Takafumi Bao, Yusheng Rivers, Samuel Bernard, Sheilah A. Shemin, Richard J. |
| description | Background. This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium.
Methods. In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4 = normal to −1 = dyskinesia), and infarct size (area of necrosis versus area at risk).
Results. After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1% ± 0.09% versus 7.8% ± 0.04%, respectively;
p < 0.002), less myocardial acidosis (−0.41 ± 0.03 versus −0.72 ± 0.03, respectively;
p < 0.0001), higher wall motion scores (3.1 ± 0.09 versus 1.67 ± 0.16, respectively;
p < 0.0001), and smaller infarct size (24.6% ± 2.0% versus 41% ± 1.3%, respectively;
p < 0.0001).
Conclusions. Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium. |
| doi_str_mv | 10.1016/S0003-4975(98)00021-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_79816965</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0003497598000216</els_id><sourcerecordid>79816965</sourcerecordid><originalsourceid>FETCH-LOGICAL-c471t-597488c0401b1482f75e7233ad28957a770f246a00cb67674376d07817477b4b3</originalsourceid><addsrcrecordid>eNqFkE1P3DAQhi3UCraUn4DkQ1W1hxTb8Ud8qqqlHystQgJ6No4zAaM4Tu0Eafn1hN3VXnsajeZ5Z0YPQueUfKOEyotbQkhZcK3EF119nRtGC3mEFlQIVkgm9Du0OCAn6EPOT1tIiGN0rIXkmrIFur-N3VR3gJcxDB0E6Ed8Aw6GMSZ8txkAr_DaBz9mfGmDfQB8OSXfP8zQs81u6mzyL3b0scexxavsHiF4h6820dnU-Cl8RO9b22U429dT9PfXz7vln2J9_Xu1_LEuHFd0LIRWvKoc4YTWlFesVQIUK0vbsEoLZZUiLePSEuJqqaTipZINURVVXKma1-Up-rzbO6T4b4I8muCzg66zPcQpG6UrKrUUMyh2oEsx5wStGZIPNm0MJebNrNmaNW_ajK7MVpqRc-58f2CqAzSH1F7lPP-0n89ebNcm2zufDxhjlCtOZ-z7DoNZxrOHZLLz0DtofAI3mib6_zzyCnnFk38</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>79816965</pqid></control><display><type>article</type><title>Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Lazar, Harold L. ; Hamasaki, Takafumi ; Bao, Yusheng ; Rivers, Samuel ; Bernard, Sheilah A. ; Shemin, Richard J.</creator><creatorcontrib>Lazar, Harold L. ; Hamasaki, Takafumi ; Bao, Yusheng ; Rivers, Samuel ; Bernard, Sheilah A. ; Shemin, Richard J.</creatorcontrib><description>Background. This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium.
Methods. In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4 = normal to −1 = dyskinesia), and infarct size (area of necrosis versus area at risk).
Results. After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1% ± 0.09% versus 7.8% ± 0.04%, respectively;
p < 0.002), less myocardial acidosis (−0.41 ± 0.03 versus −0.72 ± 0.03, respectively;
p < 0.0001), higher wall motion scores (3.1 ± 0.09 versus 1.67 ± 0.16, respectively;
p < 0.0001), and smaller infarct size (24.6% ± 2.0% versus 41% ± 1.3%, respectively;
p < 0.0001).
Conclusions. Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.</description><identifier>ISSN: 0003-4975</identifier><identifier>EISSN: 1552-6259</identifier><identifier>DOI: 10.1016/S0003-4975(98)00021-6</identifier><identifier>PMID: 9564912</identifier><identifier>CODEN: ATHSAK</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Acidosis - etiology ; Acidosis - physiopathology ; Animals ; Biological and medical sciences ; Cardiomyopathies - etiology ; Cardiomyopathies - physiopathology ; Cardiovascular system ; Complement Activation - drug effects ; Complement Inactivator Proteins - administration & dosage ; Complement Inactivator Proteins - therapeutic use ; Coronary Disease - physiopathology ; Heart Arrest, Induced ; Hemolysis ; Humans ; Hydrogen-Ion Concentration ; Infusions, Intravenous ; Medical sciences ; Miscellaneous ; Myocardial Contraction - drug effects ; Myocardial Ischemia - pathology ; Myocardial Ischemia - physiopathology ; Myocardial Ischemia - therapy ; Myocardial Reperfusion ; Myocardial Reperfusion Injury - prevention & control ; Myocardium - pathology ; Necrosis ; Pharmacology. Drug treatments ; Random Allocation ; Receptors, Complement - administration & dosage ; Receptors, Complement - therapeutic use ; Swine</subject><ispartof>The Annals of thoracic surgery, 1998-04, Vol.65 (4), p.973-977</ispartof><rights>1998 The Society of Thoracic Surgeons</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-597488c0401b1482f75e7233ad28957a770f246a00cb67674376d07817477b4b3</citedby><cites>FETCH-LOGICAL-c471t-597488c0401b1482f75e7233ad28957a770f246a00cb67674376d07817477b4b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0003497598000216$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2214741$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9564912$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lazar, Harold L.</creatorcontrib><creatorcontrib>Hamasaki, Takafumi</creatorcontrib><creatorcontrib>Bao, Yusheng</creatorcontrib><creatorcontrib>Rivers, Samuel</creatorcontrib><creatorcontrib>Bernard, Sheilah A.</creatorcontrib><creatorcontrib>Shemin, Richard J.</creatorcontrib><title>Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium</title><title>The Annals of thoracic surgery</title><addtitle>Ann Thorac Surg</addtitle><description>Background. This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium.
Methods. In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4 = normal to −1 = dyskinesia), and infarct size (area of necrosis versus area at risk).
Results. After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1% ± 0.09% versus 7.8% ± 0.04%, respectively;
p < 0.002), less myocardial acidosis (−0.41 ± 0.03 versus −0.72 ± 0.03, respectively;
p < 0.0001), higher wall motion scores (3.1 ± 0.09 versus 1.67 ± 0.16, respectively;
p < 0.0001), and smaller infarct size (24.6% ± 2.0% versus 41% ± 1.3%, respectively;
p < 0.0001).
Conclusions. Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.</description><subject>Acidosis - etiology</subject><subject>Acidosis - physiopathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiomyopathies - etiology</subject><subject>Cardiomyopathies - physiopathology</subject><subject>Cardiovascular system</subject><subject>Complement Activation - drug effects</subject><subject>Complement Inactivator Proteins - administration & dosage</subject><subject>Complement Inactivator Proteins - therapeutic use</subject><subject>Coronary Disease - physiopathology</subject><subject>Heart Arrest, Induced</subject><subject>Hemolysis</subject><subject>Humans</subject><subject>Hydrogen-Ion Concentration</subject><subject>Infusions, Intravenous</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardial Ischemia - therapy</subject><subject>Myocardial Reperfusion</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocardium - pathology</subject><subject>Necrosis</subject><subject>Pharmacology. Drug treatments</subject><subject>Random Allocation</subject><subject>Receptors, Complement - administration & dosage</subject><subject>Receptors, Complement - therapeutic use</subject><subject>Swine</subject><issn>0003-4975</issn><issn>1552-6259</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1P3DAQhi3UCraUn4DkQ1W1hxTb8Ud8qqqlHystQgJ6No4zAaM4Tu0Eafn1hN3VXnsajeZ5Z0YPQueUfKOEyotbQkhZcK3EF119nRtGC3mEFlQIVkgm9Du0OCAn6EPOT1tIiGN0rIXkmrIFur-N3VR3gJcxDB0E6Ed8Aw6GMSZ8txkAr_DaBz9mfGmDfQB8OSXfP8zQs81u6mzyL3b0scexxavsHiF4h6820dnU-Cl8RO9b22U429dT9PfXz7vln2J9_Xu1_LEuHFd0LIRWvKoc4YTWlFesVQIUK0vbsEoLZZUiLePSEuJqqaTipZINURVVXKma1-Up-rzbO6T4b4I8muCzg66zPcQpG6UrKrUUMyh2oEsx5wStGZIPNm0MJebNrNmaNW_ajK7MVpqRc-58f2CqAzSH1F7lPP-0n89ebNcm2zufDxhjlCtOZ-z7DoNZxrOHZLLz0DtofAI3mib6_zzyCnnFk38</recordid><startdate>19980401</startdate><enddate>19980401</enddate><creator>Lazar, Harold L.</creator><creator>Hamasaki, Takafumi</creator><creator>Bao, Yusheng</creator><creator>Rivers, Samuel</creator><creator>Bernard, Sheilah A.</creator><creator>Shemin, Richard J.</creator><general>Elsevier Inc</general><general>Elsevier Science</general><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>7X8</scope></search><sort><creationdate>19980401</creationdate><title>Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium</title><author>Lazar, Harold L. ; Hamasaki, Takafumi ; Bao, Yusheng ; Rivers, Samuel ; Bernard, Sheilah A. ; Shemin, Richard J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-597488c0401b1482f75e7233ad28957a770f246a00cb67674376d07817477b4b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acidosis - etiology</topic><topic>Acidosis - physiopathology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiomyopathies - etiology</topic><topic>Cardiomyopathies - physiopathology</topic><topic>Cardiovascular system</topic><topic>Complement Activation - drug effects</topic><topic>Complement Inactivator Proteins - administration & dosage</topic><topic>Complement Inactivator Proteins - therapeutic use</topic><topic>Coronary Disease - physiopathology</topic><topic>Heart Arrest, Induced</topic><topic>Hemolysis</topic><topic>Humans</topic><topic>Hydrogen-Ion Concentration</topic><topic>Infusions, Intravenous</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Ischemia - pathology</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Myocardial Ischemia - therapy</topic><topic>Myocardial Reperfusion</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocardium - pathology</topic><topic>Necrosis</topic><topic>Pharmacology. Drug treatments</topic><topic>Random Allocation</topic><topic>Receptors, Complement - administration & dosage</topic><topic>Receptors, Complement - therapeutic use</topic><topic>Swine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lazar, Harold L.</creatorcontrib><creatorcontrib>Hamasaki, Takafumi</creatorcontrib><creatorcontrib>Bao, Yusheng</creatorcontrib><creatorcontrib>Rivers, Samuel</creatorcontrib><creatorcontrib>Bernard, Sheilah A.</creatorcontrib><creatorcontrib>Shemin, Richard J.</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>The Annals of thoracic surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lazar, Harold L.</au><au>Hamasaki, Takafumi</au><au>Bao, Yusheng</au><au>Rivers, Samuel</au><au>Bernard, Sheilah A.</au><au>Shemin, Richard J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium</atitle><jtitle>The Annals of thoracic surgery</jtitle><addtitle>Ann Thorac Surg</addtitle><date>1998-04-01</date><risdate>1998</risdate><volume>65</volume><issue>4</issue><spage>973</spage><epage>977</epage><pages>973-977</pages><issn>0003-4975</issn><eissn>1552-6259</eissn><coden>ATHSAK</coden><abstract>Background. This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium.
Methods. In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4 = normal to −1 = dyskinesia), and infarct size (area of necrosis versus area at risk).
Results. After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1% ± 0.09% versus 7.8% ± 0.04%, respectively;
p < 0.002), less myocardial acidosis (−0.41 ± 0.03 versus −0.72 ± 0.03, respectively;
p < 0.0001), higher wall motion scores (3.1 ± 0.09 versus 1.67 ± 0.16, respectively;
p < 0.0001), and smaller infarct size (24.6% ± 2.0% versus 41% ± 1.3%, respectively;
p < 0.0001).
Conclusions. Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>9564912</pmid><doi>10.1016/S0003-4975(98)00021-6</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Acidosis - etiology Acidosis - physiopathology Animals Biological and medical sciences Cardiomyopathies - etiology Cardiomyopathies - physiopathology Cardiovascular system Complement Activation - drug effects Complement Inactivator Proteins - administration & dosage Complement Inactivator Proteins - therapeutic use Coronary Disease - physiopathology Heart Arrest, Induced Hemolysis Humans Hydrogen-Ion Concentration Infusions, Intravenous Medical sciences Miscellaneous Myocardial Contraction - drug effects Myocardial Ischemia - pathology Myocardial Ischemia - physiopathology Myocardial Ischemia - therapy Myocardial Reperfusion Myocardial Reperfusion Injury - prevention & control Myocardium - pathology Necrosis Pharmacology. Drug treatments Random Allocation Receptors, Complement - administration & dosage Receptors, Complement - therapeutic use Swine |
| title | Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium |
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