Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation

Complement activation during extracorporeal membrane oxygenation (ECMO) in newborns can be caused by both the underlying disease processes and by blood contact with the ECMO circuit. We investigated the relative importance of these mechanisms by measuring C3a, C5a and sC5b-9 before, during and after...

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Main Authors: Johannes Graulich, Joseph Sonntag, Monika Marcinkowski, Karl Bauer, Hans Kössel, Christoph Bührer, Michael Obladen, Hans T. Versmold
Format: Article
Language:English
Published: Wiley 2002-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1080/09629350220131908
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author Johannes Graulich
Joseph Sonntag
Monika Marcinkowski
Karl Bauer
Hans Kössel
Christoph Bührer
Michael Obladen
Hans T. Versmold
author_facet Johannes Graulich
Joseph Sonntag
Monika Marcinkowski
Karl Bauer
Hans Kössel
Christoph Bührer
Michael Obladen
Hans T. Versmold
author_sort Johannes Graulich
collection DOAJ
description Complement activation during extracorporeal membrane oxygenation (ECMO) in newborns can be caused by both the underlying disease processes and by blood contact with the ECMO circuit. We investigated the relative importance of these mechanisms by measuring C3a, C5a and sC5b-9 before, during and after neonatal ECMO in six consecutive newborn patients using enzyme-linked immunoassay. In addition complement activation during in vitro ECMO with repeated flow of the same blood volume was measured using blood from healthy adult donors. C3a increased significantly in vivo after 1 h (from 1035 ± 193 to 1865 ± 419 μg/l) and in vitro ECMO (from 314 ± 75 to 1962 ± 1062 μg/l). C5a increased during ECMO without significant differences between in vivo and in vitro activation. In neonatal patients, sC5b-9 rose faster than in vitro, but the rapid increase was also significant for in vitro experiments (in vivo: from 328 ± 63 to 1623 ± 387 μg/l after 2 h; and in vitro: from 78 ± 32 to 453 ± 179 μg/l after 8 h). After this initial peak at 1-2 h, complement activation decreased gradually until 2-3 days after the initiation of ECMO. We conclude that in newborns the rapid activation of the complement system after the start of ECMO is predominantly caused by contact with artificial surfaces rather than the patient's underlying disease.
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spelling doaj-art-e3c07a34dd5241bebccb5f17d176e40c2025-02-03T00:59:31ZengWileyMediators of Inflammation0962-93511466-18612002-01-01112697310.1080/09629350220131908Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenationJohannes Graulich0Joseph Sonntag1Monika Marcinkowski2Karl Bauer3Hans Kössel4Christoph Bührer5Michael Obladen6Hans T. Versmold7Department of Neonatology, Charité School of Medicine, Campus Virchow Klinikum, Humboldt Universität, Berlin D-13353, GermanyDepartment of Neonatology, Charité School of Medicine, Campus Virchow Klinikum, Humboldt Universität, Berlin D-13353, GermanyDepartment of Pediatrics, Universitätsklinikum Benjamin Franklin, Free University Berlin, Berlin D-12200, GermanyDepartment of Pediatrics, Universitätsklinikum Benjamin Franklin, Free University Berlin, Berlin D-12200, GermanyDepartment of Pediatrics, Universitätsklinikum Benjamin Franklin, Free University Berlin, Berlin D-12200, GermanyDepartment of Neonatology, Charité School of Medicine, Campus Virchow Klinikum, Humboldt Universität, Berlin D-13353, GermanyDepartment of Neonatology, Charité School of Medicine, Campus Virchow Klinikum, Humboldt Universität, Berlin D-13353, GermanyDepartment of Pediatrics, Universitätsklinikum Benjamin Franklin, Free University Berlin, Berlin D-12200, GermanyComplement activation during extracorporeal membrane oxygenation (ECMO) in newborns can be caused by both the underlying disease processes and by blood contact with the ECMO circuit. We investigated the relative importance of these mechanisms by measuring C3a, C5a and sC5b-9 before, during and after neonatal ECMO in six consecutive newborn patients using enzyme-linked immunoassay. In addition complement activation during in vitro ECMO with repeated flow of the same blood volume was measured using blood from healthy adult donors. C3a increased significantly in vivo after 1 h (from 1035 ± 193 to 1865 ± 419 μg/l) and in vitro ECMO (from 314 ± 75 to 1962 ± 1062 μg/l). C5a increased during ECMO without significant differences between in vivo and in vitro activation. In neonatal patients, sC5b-9 rose faster than in vitro, but the rapid increase was also significant for in vitro experiments (in vivo: from 328 ± 63 to 1623 ± 387 μg/l after 2 h; and in vitro: from 78 ± 32 to 453 ± 179 μg/l after 8 h). After this initial peak at 1-2 h, complement activation decreased gradually until 2-3 days after the initiation of ECMO. We conclude that in newborns the rapid activation of the complement system after the start of ECMO is predominantly caused by contact with artificial surfaces rather than the patient's underlying disease.http://dx.doi.org/10.1080/09629350220131908
spellingShingle Johannes Graulich
Joseph Sonntag
Monika Marcinkowski
Karl Bauer
Hans Kössel
Christoph Bührer
Michael Obladen
Hans T. Versmold
Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation
Mediators of Inflammation
title Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation
title_full Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation
title_fullStr Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation
title_full_unstemmed Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation
title_short Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation
title_sort complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation
url http://dx.doi.org/10.1080/09629350220131908
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