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Neutrophil adhesion and the inflammatory response induced by cardiopulmonary bypass

Published online by Cambridge University Press:  19 August 2008

Adam Finn
Affiliation:
Department of Paediatrics, Children' Hospital, the University of Sheffield, Sheffield, and the Lillie FrankHouston
William J. Dreyer*
Affiliation:
Abercrombie Section of Cardiology, the Speros P. Martel Section of Leukocyte Biology and Inflammation Research, Department of Pediatrics and the Section of Cardiovascular Sciences, Department of Medicine, Baylor College of Medicine, Houston
*
Dr. William J. Dreyer, Pediatric Cardiology, Texas Children's Hospital, 6621 Fannin, Houston, Texas 77005, USA, Tel. (713) 770-5639; Fax. (713) 770-5630.

Extract

The activation of inflammatory systems as a consequence of cardiopulmonary bypass represents one possible means by which inj ury to tissues and associated dysfunction of organs may occur in the postoperative cardiac patient, both pediatric and adult. Kirklin and colleagues demonstrated in the early 1980's that complement activation occurs as a consequence of blood exposure to the extracorporeal circuit. Subsequent studies demonstrated this to be true in systems using both bubble and membrane oxygenators. The anaphylatoxin C5a and its metabolite C5a des arg are produced during activation of the complement cascade. They are potent stimulants which may induce activation of neutrophils. This activation may be manifested as changes in shape, decreased cellular deformability, and changes in adhesive and secretory function. Activation of neutrophils by these fragments of complement could contribute to neutrophilmediated damage to tissues by promoting retention of neutrophils in vascular beds and secretion of cytotoxic substances. Recent studies demonstrating the release of neutrophil granular enzymes into the plasma following cardiopulmonary bypass are evidence that activation of neutrophils is taking place in this setting.

Type
World Forum for Pediatric Cardiology Symposium on Cardiopulmonary Bypass (Part 1)
Copyright
Copyright © Cambridge University Press 1993

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