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A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
Changes in the cytokine network and complement parameters during open heart surgery
Ivar Risnes1, Thor Ueland, Runar Lundblad
1Department of Thoracic and Cardiovascular Surgery, Rikshospitalet, University of Oslo, N-0027 Oslo, Norway. ivar.risnes@rikshospitalet.no
Insights
Cardiopulmonary bypass (CPB) triggers a complex immune response. Initial CPB phases show a rise in anti-inflammatory interleukin-10 (IL-10) and inflammatory chemokines, not just pro-inflammatory cytokines.
Area of Science:
- Immunology
- Cardiovascular Surgery
Background:
- Cardiopulmonary bypass (CPB) induces a systemic inflammatory response.
- The balance of inflammatory and anti-inflammatory mediators post-CPB is not fully understood.
Purpose of the Study:
- To investigate the cytokine network complexity after CPB.
- To analyze the balance between interleukin-10 (IL-10) and inflammatory cytokines/chemokines.
Main Methods:
- Blood samples collected from 20 patients undergoing CPB.
- Plasma levels of cytokines and complement activation markers analyzed pre- and post-CPB.
Main Results:
- Initial phase post-CPB showed increased IL-10 and inflammatory chemokines (IL-8, MCP-1).
- Tumor necrosis factor-alpha increase was modest; IL-6 remained elevated.
- Complement activation increased immediately post-CPB, returning to baseline on day one.
Conclusions:
- CPB induces a complex cytokine and complement response.
- The early phase post-CPB is characterized by a significant rise in anti-inflammatory IL-10, unlike infection responses.
Objectives:
During cardiac surgery with cardiopulmonary bypass (CBP) there is a systemic inflammatory reaction, involving enhanced release of inflammatory cytokines and complement. However, few studies have analysed the levels of anti-inflammatory mediators and chemokines after CPB. In this study we investigated the complexity of the cytokine network particularly focusing on the balance between interleukin (IL)-10 and inflammatory cytokines and chemokines.
Methods:
Blood samples from 20 patients (seven females; 13 males, age 30-81 (median 65) years) who underwent CPB, were collected before, and at several time points after surgery ,and analyzed for plasma levels of inflammatory and anti-inflammatory cytokines and parameters of complement activation.
Results:
A marked increase in the anti-inflammatory cytokine IL-10, rather than in inflammatory cytokines, characterized the initial phase after CBP. As for the early inflammatory response the most prominent feature was a rise in the inflammatory chemokines IL-8 and monocyte chemoattractant protein-1, while the increase in tumor necrosis factor-alpha was rather modest. In contrast to the rapid 'rise and fall' in most of the markers, significantly raised IL-6 levels persisted throughout the study. Immediately after CPB there was also a marked increase in complement activation, with return to baseline levels on the first postoperative day.
Conclusion:
The present study shows a complex pattern of changes in the cytokine network and complement parameters during CBP with a marked rise in both inflammatory and anti-inflammatory mediators. However, in contrast to cytokine pattern during various infections, the initial phase after CPB was dominated by a marked rise in anti-inflammatory cytokines (i.e. IL-10).
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