Sublytic complement attack reduces infarct size in rabbit isolated hearts: evidence for C5a-mediated cardioprotection

Sublytic complement attack can elicit protective cellular responses without precipitating cell death. Our investigation examined the effects of non-lethal complement activation in isolated hearts. New Zealand white rabbit hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion. Pr...

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Veröffentlicht in:Immunopharmacology 2000-09, Vol.49 (3), p.391-399
Hauptverfasser: Tanhehco, Elaine J, Lee, Heekyung, Lucchesi, Benedict R
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creator Tanhehco, Elaine J
Lee, Heekyung
Lucchesi, Benedict R
description Sublytic complement attack can elicit protective cellular responses without precipitating cell death. Our investigation examined the effects of non-lethal complement activation in isolated hearts. New Zealand white rabbit hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion. Prior to ischemia, hearts were perfused for 20 min with 0.5% normal human plasma (NHP). Hearts treated with NHP developed significantly (p
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Our investigation examined the effects of non-lethal complement activation in isolated hearts. New Zealand white rabbit hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion. Prior to ischemia, hearts were perfused for 20 min with 0.5% normal human plasma (NHP). Hearts treated with NHP developed significantly (p&lt;0.05) smaller infarcts compared with controls, expressed as percent of area at risk (AAR) (25.3±4.0% vs. 40.9±4.3%, respectively). Heat-inactivation, soluble complement receptor 1 (sCR1; 20 nM), and anti-C5a antibody reversed the protective effect of NHP (39.0±3.1%, 41.7±5.1% and 38.4±2.3% AAR, respectively). Hearts treated with 3 nM C5a exhibited infarct sizes similar to those exposed to NHP (27.6±5.0% AAR). sCR1 alone did not affect infarct size (37.9±4.5% AAR). The results suggest that non-lethal complement activation attenuates reperfusion injury through formation of C5a.</description><identifier>ISSN: 0162-3109</identifier><identifier>DOI: 10.1016/S0162-3109(00)00258-7</identifier><identifier>PMID: 10996036</identifier><identifier>CODEN: IMMUDP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Anaphylatoxin ; Animals ; Antianginal agents. Coronary vasodilator agents ; Biological and medical sciences ; Cardiovascular system ; Complement Activation - immunology ; Complement C5a - physiology ; complement component C5a ; Complement Membrane Attack Complex - physiology ; Hemodynamics - immunology ; Hemolysis - immunology ; Humans ; In Vitro Techniques ; Ischemia/reperfusion ; Male ; Medical sciences ; Myocardial Infarction - immunology ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Myocardial Infarction - prevention &amp; control ; Myocardial Reperfusion ; Pharmacology. 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Our investigation examined the effects of non-lethal complement activation in isolated hearts. New Zealand white rabbit hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion. Prior to ischemia, hearts were perfused for 20 min with 0.5% normal human plasma (NHP). Hearts treated with NHP developed significantly (p&lt;0.05) smaller infarcts compared with controls, expressed as percent of area at risk (AAR) (25.3±4.0% vs. 40.9±4.3%, respectively). Heat-inactivation, soluble complement receptor 1 (sCR1; 20 nM), and anti-C5a antibody reversed the protective effect of NHP (39.0±3.1%, 41.7±5.1% and 38.4±2.3% AAR, respectively). Hearts treated with 3 nM C5a exhibited infarct sizes similar to those exposed to NHP (27.6±5.0% AAR). sCR1 alone did not affect infarct size (37.9±4.5% AAR). The results suggest that non-lethal complement activation attenuates reperfusion injury through formation of C5a.</description><subject>Anaphylatoxin</subject><subject>Animals</subject><subject>Antianginal agents. Coronary vasodilator agents</subject><subject>Biological and medical sciences</subject><subject>Cardiovascular system</subject><subject>Complement Activation - immunology</subject><subject>Complement C5a - physiology</subject><subject>complement component C5a</subject><subject>Complement Membrane Attack Complex - physiology</subject><subject>Hemodynamics - immunology</subject><subject>Hemolysis - immunology</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Ischemia/reperfusion</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - immunology</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial Infarction - prevention &amp; control</subject><subject>Myocardial Reperfusion</subject><subject>Pharmacology. Drug treatments</subject><subject>Rabbits</subject><subject>Receptors, Complement 3b - physiology</subject><subject>Solubility</subject><subject>Soluble complement receptor 1</subject><issn>0162-3109</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1TAQhb0A0VJ4BJAXCJVFqJ04dswGoSsKSJVYtKytiT0WhiS-2E6l8vT1_VFh141HHn0zZ3QOIa84e88ZlxfX9WmbjjN9ztg7xtp-aNQTcvrQPiHPc_7FGBNK98_ISW1pyTp5StbrdZzuSrDUxnk74YxLoVAK2N80oVstZhoWD8kWmsNfrB-aYBxDoSHHCQo6-hMhlfyB4m1wuFikPia66aGZ0YU9YSG5ELcpFrQlxOUFeephyvjyWM_Ij8vPN5uvzdX3L982n64aK1pemm4QSo7aKYEMlOB6aKUYHXfaCw69A9EJznuvGPPawmilFq4bPW_r5MC77oy8Peyt0n9WzMXMIVucJlgwrtmoth0kl-pRkKuh14MeKtgfQJtizgm92aYwQ7oznJldGGYfhtm5bhgz-zDMTuD1UWAdqy3_TR2SqMCbIwDZwuQTLDbkf1zPuZK6Yh8PGFbbbgMmk23Yme5Cqt4aF8Mjl9wDENGowA</recordid><startdate>20000901</startdate><enddate>20000901</enddate><creator>Tanhehco, Elaine J</creator><creator>Lee, Heekyung</creator><creator>Lucchesi, Benedict R</creator><general>Elsevier B.V</general><general>Elsevier</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20000901</creationdate><title>Sublytic complement attack reduces infarct size in rabbit isolated hearts: evidence for C5a-mediated cardioprotection</title><author>Tanhehco, Elaine J ; Lee, Heekyung ; Lucchesi, Benedict R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-38476b9d74e0a74198264bd1d9f41a5da434115f700f9cabc694d3bf123848133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Anaphylatoxin</topic><topic>Animals</topic><topic>Antianginal agents. Coronary vasodilator agents</topic><topic>Biological and medical sciences</topic><topic>Cardiovascular system</topic><topic>Complement Activation - immunology</topic><topic>Complement C5a - physiology</topic><topic>complement component C5a</topic><topic>Complement Membrane Attack Complex - physiology</topic><topic>Hemodynamics - immunology</topic><topic>Hemolysis - immunology</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Ischemia/reperfusion</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - immunology</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial Infarction - prevention &amp; control</topic><topic>Myocardial Reperfusion</topic><topic>Pharmacology. Drug treatments</topic><topic>Rabbits</topic><topic>Receptors, Complement 3b - physiology</topic><topic>Solubility</topic><topic>Soluble complement receptor 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tanhehco, Elaine J</creatorcontrib><creatorcontrib>Lee, Heekyung</creatorcontrib><creatorcontrib>Lucchesi, Benedict R</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tanhehco, Elaine J</au><au>Lee, Heekyung</au><au>Lucchesi, Benedict R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sublytic complement attack reduces infarct size in rabbit isolated hearts: evidence for C5a-mediated cardioprotection</atitle><jtitle>Immunopharmacology</jtitle><addtitle>Immunopharmacology</addtitle><date>2000-09-01</date><risdate>2000</risdate><volume>49</volume><issue>3</issue><spage>391</spage><epage>399</epage><pages>391-399</pages><issn>0162-3109</issn><coden>IMMUDP</coden><abstract>Sublytic complement attack can elicit protective cellular responses without precipitating cell death. Our investigation examined the effects of non-lethal complement activation in isolated hearts. New Zealand white rabbit hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion. Prior to ischemia, hearts were perfused for 20 min with 0.5% normal human plasma (NHP). Hearts treated with NHP developed significantly (p&lt;0.05) smaller infarcts compared with controls, expressed as percent of area at risk (AAR) (25.3±4.0% vs. 40.9±4.3%, respectively). Heat-inactivation, soluble complement receptor 1 (sCR1; 20 nM), and anti-C5a antibody reversed the protective effect of NHP (39.0±3.1%, 41.7±5.1% and 38.4±2.3% AAR, respectively). Hearts treated with 3 nM C5a exhibited infarct sizes similar to those exposed to NHP (27.6±5.0% AAR). sCR1 alone did not affect infarct size (37.9±4.5% AAR). The results suggest that non-lethal complement activation attenuates reperfusion injury through formation of C5a.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10996036</pmid><doi>10.1016/S0162-3109(00)00258-7</doi><tpages>9</tpages></addata></record>
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subjects Anaphylatoxin
Animals
Antianginal agents. Coronary vasodilator agents
Biological and medical sciences
Cardiovascular system
Complement Activation - immunology
Complement C5a - physiology
complement component C5a
Complement Membrane Attack Complex - physiology
Hemodynamics - immunology
Hemolysis - immunology
Humans
In Vitro Techniques
Ischemia/reperfusion
Male
Medical sciences
Myocardial Infarction - immunology
Myocardial Infarction - pathology
Myocardial Infarction - physiopathology
Myocardial Infarction - prevention & control
Myocardial Reperfusion
Pharmacology. Drug treatments
Rabbits
Receptors, Complement 3b - physiology
Solubility
Soluble complement receptor 1
title Sublytic complement attack reduces infarct size in rabbit isolated hearts: evidence for C5a-mediated cardioprotection
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