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Ann Thorac Surg 2001;71:233-237
© 2001 The Society of Thoracic Surgeons
a Department of Pediatric Intensive Care, Chaim Sheba Medical Center, Tel Hashomer, Israel
b Department of Pediatric Intensive Care, Schneider Medical Center, Petach Tikvah, Israel
c Tel-Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Accepted for publication May 5, 2000.
Address reprint requests to Dr Paret, Department of Pediatric Intensive Care, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
e-mail: gparet{at}post.tau.ac.il
Background. Surgery involving cardiopulmonary bypass (CPB) is frequently accompanied by a systemic inflammatory response partly triggered by neutrophils and monocyte-macrophages. Certain cytokines that are powerful leukocyte-chemotactic factors have recently been characterized and shown to be important in evoking inflammatory responses: monocyte chemoattractant protein-1 (MCP-1) has monocyte-macrophage chemotactic activity, and regulated-upon-activation normal T-cell expressed and secreted (RANTES) has a potent chemoattractant activity for mononuclear phagocytes. This prospective cohort study investigated possible roles of these chemokines in the inflammatory response to CPB and relationships between the changes in chemokine levels and the clinical course and outcome.
Methods. Systemic blood of 16 children undergoing CPB was collected after induction of anesthesia (base line); at 15 minutes after bypass onset; at CPB cessation; and at 1, 2, 4, 8, 12, and 24 hours afterward to measure MCP-1 and RANTES.
Results. The significant changes of plasma ß chemokine levels following CPB were associated with patient characteristics, operative variables, and postoperative course. Cardiopulmonary bypass of more than 2 hours, longer surgical times, inotropic support, and reoperation were associated with higher MCP-1 levels and lower RANTES levels.
Conclusions. Our results suggest a relation between CPB-induced mediators and clinical effects, implying pathogenic roles for chemokines following CPB. These molecules should be considered as possible targets for therapeutic intervention.
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