[Activation of granulocytes and antiproteases in open heart surgery]

Cardiovascular surgical procedures with extracorporeal circulation (ECC) lead to neutrophil activation followed by the release of proteases such as neutrophil elastase (NE) and oxidants. The mis-balance between proteases and their physiological inhibitors may contribute to morbidity in the postoperative period. In this study, the effects of cardiac surgery on neutrophil mediators were evaluated. Release of neutrophil elastase and plasma levels of the natural NE antagonists alpha (1)-proteinase inhibitor (API) and secretory leukocyte proteinase inhibitor (SLPI) were measured. The oxidative burst and the phagocytic activity were also evaluated. Tissue destruction was quantified by measuring the serum concentration of fibronectin.

Blood samples were obtained from 30 patients undergoing elective coronary artery bypass grafting (n = 30). NE and SLPI concentrations were measured by ELISA, API and fibronectin plasma levels were determined by nephelometry. Neutrophil phagocytic activity and oxidative burst were evaluated by flow cytometry.

Neutrophil elastase plasma concentrations rose during ECC (245 +/- 107 microg/ml versus 44 +/- 14 microg/ml after induction, p < 0.001), whereas SLPI and API were decreased after onset of ECC. 24 h after ECC SLPI (54 +/- 17 ng/ml versus 41 +/- 10 ng/ml, p < 0.05) and API (3 +/- 0.5 g/l versus 1.6 +/- 0.3 g/l, p < 0.05) increased significantly compared to baseline values. A minor increase in phagocytic activity was observed after the onset of ECC. There were no significant changes in the oxidative burst.

Cardiac surgery with ECC leads to neutrophil activation and elastase release. The imbalance between NE and the NE inhibitors API and SLPI may increase the risk for tissue damage due to granulocyte activation after cardiac surgery.