Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass : The role of tissue injury by surgical incision
Complement activation is a trigger in inducing inflammation in patients who undergo coronary artery bypass grafting (CABG) and is usually thought to be induced by the use of cardiopulmonary bypass (CPB). In this study, we examined whether tissue injury caused by chest surgical incision per se contri...
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Veröffentlicht in: | Chest 1999-10, Vol.116 (4), p.892-898 |
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description | Complement activation is a trigger in inducing inflammation in patients who undergo coronary artery bypass grafting (CABG) and is usually thought to be induced by the use of cardiopulmonary bypass (CPB). In this study, we examined whether tissue injury caused by chest surgical incision per se contributes to complement activation in CABG patients.
Prospective study.
Thorax center in university hospital.
Twenty-two patients undergoing CABG without CPB were prospectively divided into two groups: a small chest incision via an anterolateral thoracotomy representing a minimized tissue injury (lateral group, n = 8), and a conventional median sternotomy representing a large tissue injury (median group, n = 14). Biochemical markers indicating complement activation as well as systemic inflammatory response were determined before, during, and after the operation.
Plasma concentrations of complement 3a increased in both the lateral and median groups right after chest incision (p < 0.01 and p < 0.05, respectively) and by the end of operation increased only in the median group (p < 0.01). The terminal complement complex 5b-9 did not increase in the lateral group, but it did increase in the median group both after incision and by the end of the operation (p < 0.05 and p < 0.05, respectively). During surgery, complement 4a did not increase, suggesting that it is the alternative rather than the classic pathway that is involved in complement activation by tissue injury. Postoperatively, interleukin-6 production was greater in the median group (p < 0.01) than the lateral group (p < 0.05), suggesting a more pronounced inflammatory response to a larger chest incision.
Tissue injury caused by surgical incision contributes to complement activation in CABG patients who are operated on without CPB. A small anterolateral thoracotomy is associated with reduced complement activation in comparison with a median sternotomy. |
doi_str_mv | 10.1378/chest.116.4.892 |
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Prospective study.
Thorax center in university hospital.
Twenty-two patients undergoing CABG without CPB were prospectively divided into two groups: a small chest incision via an anterolateral thoracotomy representing a minimized tissue injury (lateral group, n = 8), and a conventional median sternotomy representing a large tissue injury (median group, n = 14). Biochemical markers indicating complement activation as well as systemic inflammatory response were determined before, during, and after the operation.
Plasma concentrations of complement 3a increased in both the lateral and median groups right after chest incision (p < 0.01 and p < 0.05, respectively) and by the end of operation increased only in the median group (p < 0.01). The terminal complement complex 5b-9 did not increase in the lateral group, but it did increase in the median group both after incision and by the end of the operation (p < 0.05 and p < 0.05, respectively). During surgery, complement 4a did not increase, suggesting that it is the alternative rather than the classic pathway that is involved in complement activation by tissue injury. Postoperatively, interleukin-6 production was greater in the median group (p < 0.01) than the lateral group (p < 0.05), suggesting a more pronounced inflammatory response to a larger chest incision.
Tissue injury caused by surgical incision contributes to complement activation in CABG patients who are operated on without CPB. A small anterolateral thoracotomy is associated with reduced complement activation in comparison with a median sternotomy.]]></description><identifier>ISSN: 0012-3692</identifier><identifier>EISSN: 1931-3543</identifier><identifier>DOI: 10.1378/chest.116.4.892</identifier><identifier>PMID: 10531149</identifier><identifier>CODEN: CHETBF</identifier><language>eng</language><publisher>Northbrook, IL: American College of Chest Physicians</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Cardiopulmonary Bypass ; Cardiovascular disease ; Complement Activation - immunology ; Complement C3a - metabolism ; Complement C4a - metabolism ; Complement Membrane Attack Complex - metabolism ; Coronary Artery Bypass ; Coronary vessels ; Cytokines ; Female ; Heart surgery ; Hospitals, University ; Humans ; Interleukin-6 - blood ; Intraoperative Period ; Male ; Medical sciences ; Middle Aged ; Netherlands ; Ostomy ; Postoperative Complications - immunology ; Prospective Studies ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; Sutures ; Systemic Inflammatory Response Syndrome - immunology ; Thoracotomy</subject><ispartof>Chest, 1999-10, Vol.116 (4), p.892-898</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American College of Chest Physicians Oct 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1968128$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10531149$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GU, Y. J</creatorcontrib><creatorcontrib>MARIANI, M. A</creatorcontrib><creatorcontrib>BOONSTRA, P. W</creatorcontrib><creatorcontrib>GRANDJEAN, J. G</creatorcontrib><creatorcontrib>VAN OEVEREN, W</creatorcontrib><title>Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass : The role of tissue injury by surgical incision</title><title>Chest</title><addtitle>Chest</addtitle><description><![CDATA[Complement activation is a trigger in inducing inflammation in patients who undergo coronary artery bypass grafting (CABG) and is usually thought to be induced by the use of cardiopulmonary bypass (CPB). In this study, we examined whether tissue injury caused by chest surgical incision per se contributes to complement activation in CABG patients.
Prospective study.
Thorax center in university hospital.
Twenty-two patients undergoing CABG without CPB were prospectively divided into two groups: a small chest incision via an anterolateral thoracotomy representing a minimized tissue injury (lateral group, n = 8), and a conventional median sternotomy representing a large tissue injury (median group, n = 14). Biochemical markers indicating complement activation as well as systemic inflammatory response were determined before, during, and after the operation.
Plasma concentrations of complement 3a increased in both the lateral and median groups right after chest incision (p < 0.01 and p < 0.05, respectively) and by the end of operation increased only in the median group (p < 0.01). The terminal complement complex 5b-9 did not increase in the lateral group, but it did increase in the median group both after incision and by the end of the operation (p < 0.05 and p < 0.05, respectively). During surgery, complement 4a did not increase, suggesting that it is the alternative rather than the classic pathway that is involved in complement activation by tissue injury. Postoperatively, interleukin-6 production was greater in the median group (p < 0.01) than the lateral group (p < 0.05), suggesting a more pronounced inflammatory response to a larger chest incision.
Tissue injury caused by surgical incision contributes to complement activation in CABG patients who are operated on without CPB. A small anterolateral thoracotomy is associated with reduced complement activation in comparison with a median sternotomy.]]></description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Cardiopulmonary Bypass</subject><subject>Cardiovascular disease</subject><subject>Complement Activation - immunology</subject><subject>Complement C3a - metabolism</subject><subject>Complement C4a - metabolism</subject><subject>Complement Membrane Attack Complex - metabolism</subject><subject>Coronary Artery Bypass</subject><subject>Coronary vessels</subject><subject>Cytokines</subject><subject>Female</subject><subject>Heart surgery</subject><subject>Hospitals, University</subject><subject>Humans</subject><subject>Interleukin-6 - blood</subject><subject>Intraoperative Period</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Netherlands</subject><subject>Ostomy</subject><subject>Postoperative Complications - immunology</subject><subject>Prospective Studies</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. 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J ; MARIANI, M. A ; BOONSTRA, P. W ; GRANDJEAN, J. 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J</au><au>MARIANI, M. A</au><au>BOONSTRA, P. W</au><au>GRANDJEAN, J. G</au><au>VAN OEVEREN, W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass : The role of tissue injury by surgical incision</atitle><jtitle>Chest</jtitle><addtitle>Chest</addtitle><date>1999-10-01</date><risdate>1999</risdate><volume>116</volume><issue>4</issue><spage>892</spage><epage>898</epage><pages>892-898</pages><issn>0012-3692</issn><eissn>1931-3543</eissn><coden>CHETBF</coden><abstract><![CDATA[Complement activation is a trigger in inducing inflammation in patients who undergo coronary artery bypass grafting (CABG) and is usually thought to be induced by the use of cardiopulmonary bypass (CPB). In this study, we examined whether tissue injury caused by chest surgical incision per se contributes to complement activation in CABG patients.
Prospective study.
Thorax center in university hospital.
Twenty-two patients undergoing CABG without CPB were prospectively divided into two groups: a small chest incision via an anterolateral thoracotomy representing a minimized tissue injury (lateral group, n = 8), and a conventional median sternotomy representing a large tissue injury (median group, n = 14). Biochemical markers indicating complement activation as well as systemic inflammatory response were determined before, during, and after the operation.
Plasma concentrations of complement 3a increased in both the lateral and median groups right after chest incision (p < 0.01 and p < 0.05, respectively) and by the end of operation increased only in the median group (p < 0.01). The terminal complement complex 5b-9 did not increase in the lateral group, but it did increase in the median group both after incision and by the end of the operation (p < 0.05 and p < 0.05, respectively). During surgery, complement 4a did not increase, suggesting that it is the alternative rather than the classic pathway that is involved in complement activation by tissue injury. Postoperatively, interleukin-6 production was greater in the median group (p < 0.01) than the lateral group (p < 0.05), suggesting a more pronounced inflammatory response to a larger chest incision.
Tissue injury caused by surgical incision contributes to complement activation in CABG patients who are operated on without CPB. A small anterolateral thoracotomy is associated with reduced complement activation in comparison with a median sternotomy.]]></abstract><cop>Northbrook, IL</cop><pub>American College of Chest Physicians</pub><pmid>10531149</pmid><doi>10.1378/chest.116.4.892</doi><tpages>7</tpages></addata></record> |
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subjects | Adult Aged Biological and medical sciences Cardiopulmonary Bypass Cardiovascular disease Complement Activation - immunology Complement C3a - metabolism Complement C4a - metabolism Complement Membrane Attack Complex - metabolism Coronary Artery Bypass Coronary vessels Cytokines Female Heart surgery Hospitals, University Humans Interleukin-6 - blood Intraoperative Period Male Medical sciences Middle Aged Netherlands Ostomy Postoperative Complications - immunology Prospective Studies Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart Sutures Systemic Inflammatory Response Syndrome - immunology Thoracotomy |
title | Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass : The role of tissue injury by surgical incision |
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