Cardiac Anaphylaxis Complement Activation As an Amplification System
Complement is activated, and C3a and C5a anaphylatoxins are generated during hypersensitivity reactions clinically associated with cardlopulmonary collapse. The administration of C3a or C5a to nonsensitized isolated guinea pig hearts mimics the events caused by antigen challenge of sensitized hearts...
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Veröffentlicht in: | Circulation research 1989-09, Vol.65 (3), p.847-857 |
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description | Complement is activated, and C3a and C5a anaphylatoxins are generated during hypersensitivity reactions clinically associated with cardlopulmonary collapse. The administration of C3a or C5a to nonsensitized isolated guinea pig hearts mimics the events caused by antigen challenge of sensitized hearts (i.e., cardiac anaphylaxis) in the absence of complement. Thus, complementderived anaphylatoxins may participate in immediate hypersensitivity reactions in which the heart is a target organ. To assess the contribution of complement activation and anaphylatoxin generation to cardiac dysfunction, we have elicited anaphylaxis in isolated guinea pig hearts in the presence of complement and found that the ensuing dysfunction is markedly enhanced. This amplification is most likely attributable to anaphylatoxin formation because 1) inactivation of C3 or selective C3 depletion, i.e., the loss of the component responsible for the formation of the anaphylatoxins C3a and C5a, prevents complement-induced exacerbation of cardiac anaphylaxis, whereas reconstitution with C3 and C5, or even only C3, restores it; in fact, the greater the C3 content at the time of antigen challenge, the more intense the anaphylactic crisis; and 2) the severity of cardiac anaphylaxis is markedly reduced by preexposure to C3a, and this redaction is directly related to the dose of C3a injected and to the amount of endogenous cardiac histamine depleted by C3a before antigen challenge. Complement-derived anaphylatoxins appear to promote the same mediator release that has been initiated by the antigen-antibody reaction; thus, complement activation functions as an amplification system in cardiac anaphylaxis. |
doi_str_mv | 10.1161/01.res.65.3.847 |
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The administration of C3a or C5a to nonsensitized isolated guinea pig hearts mimics the events caused by antigen challenge of sensitized hearts (i.e., cardiac anaphylaxis) in the absence of complement. Thus, complementderived anaphylatoxins may participate in immediate hypersensitivity reactions in which the heart is a target organ. To assess the contribution of complement activation and anaphylatoxin generation to cardiac dysfunction, we have elicited anaphylaxis in isolated guinea pig hearts in the presence of complement and found that the ensuing dysfunction is markedly enhanced. This amplification is most likely attributable to anaphylatoxin formation because 1) inactivation of C3 or selective C3 depletion, i.e., the loss of the component responsible for the formation of the anaphylatoxins C3a and C5a, prevents complement-induced exacerbation of cardiac anaphylaxis, whereas reconstitution with C3 and C5, or even only C3, restores it; in fact, the greater the C3 content at the time of antigen challenge, the more intense the anaphylactic crisis; and 2) the severity of cardiac anaphylaxis is markedly reduced by preexposure to C3a, and this redaction is directly related to the dose of C3a injected and to the amount of endogenous cardiac histamine depleted by C3a before antigen challenge. Complement-derived anaphylatoxins appear to promote the same mediator release that has been initiated by the antigen-antibody reaction; thus, complement activation functions as an amplification system in cardiac anaphylaxis.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.65.3.847</identifier><identifier>PMID: 2475275</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Anaphylatoxins ; Anaphylaxis ; Animals ; Biological and medical sciences ; Complement Activation ; Complement C3 - immunology ; Complement C3a ; Complement C5 - immunology ; Complement C5a ; Coronary Circulation ; Experimental and animal immunopathology. Animal models ; Guinea Pigs ; Heart - physiopathology ; Histamine Release ; Immunopathology ; Male ; Medical sciences ; Myocardial Contraction ; Myocardium - immunology</subject><ispartof>Circulation research, 1989-09, Vol.65 (3), p.847-857</ispartof><rights>1989 American Heart Association, Inc.</rights><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5090-4bb1326100a82c16330fddfd17fd8e316a80be1c72562aecb5d6ddeb72fde6833</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7373579$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2475275$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>del Balzo, Ughetta</creatorcontrib><creatorcontrib>Polley, Margaret J</creatorcontrib><creatorcontrib>Levi, Roberto</creatorcontrib><title>Cardiac Anaphylaxis Complement Activation As an Amplification System</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Complement is activated, and C3a and C5a anaphylatoxins are generated during hypersensitivity reactions clinically associated with cardlopulmonary collapse. The administration of C3a or C5a to nonsensitized isolated guinea pig hearts mimics the events caused by antigen challenge of sensitized hearts (i.e., cardiac anaphylaxis) in the absence of complement. Thus, complementderived anaphylatoxins may participate in immediate hypersensitivity reactions in which the heart is a target organ. To assess the contribution of complement activation and anaphylatoxin generation to cardiac dysfunction, we have elicited anaphylaxis in isolated guinea pig hearts in the presence of complement and found that the ensuing dysfunction is markedly enhanced. This amplification is most likely attributable to anaphylatoxin formation because 1) inactivation of C3 or selective C3 depletion, i.e., the loss of the component responsible for the formation of the anaphylatoxins C3a and C5a, prevents complement-induced exacerbation of cardiac anaphylaxis, whereas reconstitution with C3 and C5, or even only C3, restores it; in fact, the greater the C3 content at the time of antigen challenge, the more intense the anaphylactic crisis; and 2) the severity of cardiac anaphylaxis is markedly reduced by preexposure to C3a, and this redaction is directly related to the dose of C3a injected and to the amount of endogenous cardiac histamine depleted by C3a before antigen challenge. Complement-derived anaphylatoxins appear to promote the same mediator release that has been initiated by the antigen-antibody reaction; thus, complement activation functions as an amplification system in cardiac anaphylaxis.</description><subject>Anaphylatoxins</subject><subject>Anaphylaxis</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Complement Activation</subject><subject>Complement C3 - immunology</subject><subject>Complement C3a</subject><subject>Complement C5 - immunology</subject><subject>Complement C5a</subject><subject>Coronary Circulation</subject><subject>Experimental and animal immunopathology. Animal models</subject><subject>Guinea Pigs</subject><subject>Heart - physiopathology</subject><subject>Histamine Release</subject><subject>Immunopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Contraction</subject><subject>Myocardium - immunology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kc1r3DAQxUVoSTcf55wKPpTe7MxIlmQdl036AYFC056FLMmsWtneSt6k-99X6S65zMB7vxmGN4TcIDSIAm8Bm-RzI3jDmq6VZ2SFnLZ1yyW-ISsAULVkDN6Ri5x_AWDLqDon57SVnEq-Incbk1wwtlpPZrc9RPM35Gozj7voRz8t1dou4cksYZ6qda5MqcUKQ7BH7fGQFz9ekbeDidlfn_ol-fnp_sfmS_3w7fPXzfqhthwU1G3fI6MCAUxHLYpy1-Dc4FAOrvMMhemg92gl5YIab3vuhHO-l3RwXnSMXZKPx727NP_Z-7zoMWTrYzSTn_dZS4VCKXgBb4-gTXPOyQ96l8Jo0kEj6JfcNKD-fv-oBddMl9zKxPvT6n0_evfKn4Iq_oeTb7I1cUhmsiG_YpJJxqUqWHvEnue4-JR_x_2zT3rrTVy2urwDGCCtUXWqJAJQ_1fYPxuHhTs</recordid><startdate>198909</startdate><enddate>198909</enddate><creator>del Balzo, Ughetta</creator><creator>Polley, Margaret J</creator><creator>Levi, Roberto</creator><general>American Heart Association, Inc</general><general>Lippincott</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>198909</creationdate><title>Cardiac Anaphylaxis Complement Activation As an Amplification System</title><author>del Balzo, Ughetta ; Polley, Margaret J ; Levi, Roberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5090-4bb1326100a82c16330fddfd17fd8e316a80be1c72562aecb5d6ddeb72fde6833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Anaphylatoxins</topic><topic>Anaphylaxis</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Complement Activation</topic><topic>Complement C3 - immunology</topic><topic>Complement C3a</topic><topic>Complement C5 - immunology</topic><topic>Complement C5a</topic><topic>Coronary Circulation</topic><topic>Experimental and animal immunopathology. Animal models</topic><topic>Guinea Pigs</topic><topic>Heart - physiopathology</topic><topic>Histamine Release</topic><topic>Immunopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Contraction</topic><topic>Myocardium - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>del Balzo, Ughetta</creatorcontrib><creatorcontrib>Polley, Margaret J</creatorcontrib><creatorcontrib>Levi, Roberto</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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>del Balzo, Ughetta</au><au>Polley, Margaret J</au><au>Levi, Roberto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac Anaphylaxis Complement Activation As an Amplification System</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1989-09</date><risdate>1989</risdate><volume>65</volume><issue>3</issue><spage>847</spage><epage>857</epage><pages>847-857</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Complement is activated, and C3a and C5a anaphylatoxins are generated during hypersensitivity reactions clinically associated with cardlopulmonary collapse. The administration of C3a or C5a to nonsensitized isolated guinea pig hearts mimics the events caused by antigen challenge of sensitized hearts (i.e., cardiac anaphylaxis) in the absence of complement. Thus, complementderived anaphylatoxins may participate in immediate hypersensitivity reactions in which the heart is a target organ. To assess the contribution of complement activation and anaphylatoxin generation to cardiac dysfunction, we have elicited anaphylaxis in isolated guinea pig hearts in the presence of complement and found that the ensuing dysfunction is markedly enhanced. This amplification is most likely attributable to anaphylatoxin formation because 1) inactivation of C3 or selective C3 depletion, i.e., the loss of the component responsible for the formation of the anaphylatoxins C3a and C5a, prevents complement-induced exacerbation of cardiac anaphylaxis, whereas reconstitution with C3 and C5, or even only C3, restores it; in fact, the greater the C3 content at the time of antigen challenge, the more intense the anaphylactic crisis; and 2) the severity of cardiac anaphylaxis is markedly reduced by preexposure to C3a, and this redaction is directly related to the dose of C3a injected and to the amount of endogenous cardiac histamine depleted by C3a before antigen challenge. Complement-derived anaphylatoxins appear to promote the same mediator release that has been initiated by the antigen-antibody reaction; thus, complement activation functions as an amplification system in cardiac anaphylaxis.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>2475275</pmid><doi>10.1161/01.res.65.3.847</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anaphylatoxins Anaphylaxis Animals Biological and medical sciences Complement Activation Complement C3 - immunology Complement C3a Complement C5 - immunology Complement C5a Coronary Circulation Experimental and animal immunopathology. Animal models Guinea Pigs Heart - physiopathology Histamine Release Immunopathology Male Medical sciences Myocardial Contraction Myocardium - immunology |
title | Cardiac Anaphylaxis Complement Activation As an Amplification System |
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