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Monocyte activation markers during cardiopulmonary bypass
R Fink1, M Al-Obaidi, S Grewal
1Department of Pathology, West Middlesex University Hospital, Isleworth, UK. Richard.Fink@wmuh-tr.nthames.nhs.uk
Perfusion
|July 19, 2003
Summary
Cardiac surgery triggers inflammation, impacting organs. Monocyte markers like HLA-DR decrease, while CD62L increases, potentially impairing immune function and promoting atherosclerosis post-cardiopulmonary bypass.
Area of Science:
- Immunology
- Cardiovascular Surgery
- Inflammation Research
Background:
- Extracorporeal support during cardiac surgery causes Post Pump Syndrome (PPS), an inflammatory response damaging cardiac, pulmonary, and renal tissues.
- While neutrophil and lymphocyte changes are known, the role of monocytes and their activation markers during this process is less understood.
Purpose of the Study:
- To investigate monocyte activation markers, specifically HLA-DR and CD62L, in patients undergoing cardiac surgery.
- To assess changes in these markers in aortic root and coronary sinus blood samples at different time points relative to cardiopulmonary bypass.
Main Methods:
- Blood samples were collected from 19 patients undergoing cardiac surgery from the aortic root and coronary sinus.
- Samples were taken before cardiopulmonary bypass (CPB), 1 minute after aortic crossclamp release, and 10 minutes after weaning from CPB.
- Leukocyte count, monocyte count, and activation markers (HLA-DR, CD15, CD11b, CD62L) were measured.
Main Results:
- Coronary sinus HLA-DR percentage of monocyte count significantly decreased from baseline through post-CPB periods (78%, 66%, 43%).
- A similar decrease in HLA-DR was observed in aortic root samples.
- Coronary sinus CD62L showed a marked increase (55%, 68%, 73%), with a slightly lower increase in aortic root samples (51%, 68%, 63%).
Conclusions:
- The observed decrease in HLA-DR suggests reduced monocyte immunological competence following cardiac surgery.
- Increased CD62L may sensitize monocytes to endothelial interactions, potentially contributing to the atherosclerotic process.