Complement and leukocytes during cardiopulmonary bypass: effects on plasma C3d and C5a, leukocyte count, release of
F Knudsen1, J O Pedersen, O Juhl
1Department of Anesthesia and Intensive Care, Aalborg Hospital, Denmark.
Insights
Cardiopulmonary bypass (CPB) triggers an acute inflammatory response, altering complement-leukocyte systems. This study observed changes in complement factors and impaired granulocyte migration during CPB.
Area of Science:
- Immunology
- Cardiovascular Surgery
- Hematology
Background:
- Cardiopulmonary bypass (CPB) is associated with complex inflammatory responses.
- Understanding the complement-leukocyte system's role during CPB is crucial for patient outcomes.
Purpose of the Study:
- To investigate changes in complement activation and leukocyte function during CPB.
- To elucidate the impact of CPB on the complement-leukocyte system and granulocyte migration.
Main Methods:
- Plasma levels of C3d, C5a, and granulocyte elastase bound to alpha1-proteinase inhibitor (E-alpha1 PI) were measured.
- Leukocyte counts, differential cell counts, and granulocyte migration were assessed before, during, and after CPB.
- Hemodilution was corrected for in plasma C3d measurements.
Main Results:
- Complement activation was confirmed by increased plasma C3d levels during CPB.
- Significant C5a levels were not detected.
- Plasma E-alpha1 PI increased, indicating granulocyte lysosomal enzyme release.
- Granulocyte migration was transiently impaired due to an intrinsic cellular defect.
- Leukocyte counts decreased during CPB but remained unchanged after correcting for hemodilution, except for a slight lymphocyte decrease.
- Post-CPB, neutrocytosis and lymphopenia were observed.
Conclusions:
- CPB induces acute changes in plasma and cells, mimicking a systemic inflammatory response.
- Transient impairment of granulocyte migration occurs during CPB.
- The clinical significance of these CPB-induced inflammatory changes requires further investigation.
Abstract:
In an effort to further elucidate the complex changes in the complement-leukocyte system during cardiopulmonary bypass (CPB), plasma levels of C3d, C5a, and granulocyte elastase bound to alpha1-proteinase inhibitor (E-alpha1 PI) were followed prior to, during, and after CPB. Leukocyte and differential cell counts and granulocyte migration were also determined. Complement activation was documented during CPB by an increase in plasma C3d corrected for hemodilution. Significant amounts of C5a were not revealed. Cell counts decreased during CPB but, if corrected for hemodilution, remained unchanged apart from a slight decrease in lymphocyte count after 60 minutes. Eighteen hours after CPB, neutrocytosis and lymphopenia occurred. Plasma E-alpha1 PI increased during CPB, reflecting release of granulocyte lysosomal enzymes. Granulocyte migration was transitorily depressed during CPB, and it was shown that this was due to the appearance of an intrinsic cellular defect. CPB is associated with acute changes in cells and plasma, resembling an acute whole-body inflammatory response, with transitory impairment of granulocyte migration. The clinical significance of these observations remains to be determined.
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