Different activation patterns in the plasma kallikrein-kinin and complement systems during coronary bypass surgery

Area of Science:

• Biochemistry
• Immunology
• Cardiovascular Surgery

Background:

• Cardiopulmonary bypass (CPB) during open heart surgery can trigger systemic inflammatory responses.
• The plasma kallikrein-kinin system and complement system are key mediators of inflammation and coagulation.
• Understanding their activation patterns during CPB is crucial for managing surgical outcomes.

Purpose of the Study:

• To investigate the activation kinetics of the plasma kallikrein-kinin and complement systems during open heart surgery with CPB.
• To determine the temporal relationship between heparin administration, CPB initiation, and the activation of these systems.

Main Methods:

• Measurement of spontaneous kallikrein activity (KK), plasma prekallikrein (PKK), and functional kallikrein inhibition capacity (KKI).
• Quantification of complement activation products, including C3 activation products (C3-act) and the terminal complement complex (TCC).
• Analysis of these parameters in patients undergoing open heart surgery before, during, and after CPB.

Main Results:

• Heparin injection prior to CPB induced a transient increase in KK and a decrease in PKK.
• During CPB, a further decline in PKK and KKI was observed, with levels returning to baseline postoperatively.
• Complement activation (C3-act and TCC) increased significantly after CPB initiation, with distinct patterns during and after the bypass period.

Conclusions:

• The kallikrein-kinin system is activated early, following heparin administration before CPB.
• Both the initial and terminal complement cascades are activated specifically by the onset of CPB.
• These findings highlight distinct triggers for the activation of these inflammatory systems during cardiac surgery.