Complement activation during cardiac and thoracic vascular operations.

Abstract

To study complement activation, we evaluated nine patients who underwent cardiac operations requiring cardiopulmonary bypass (CPB) and nine other patients who underwent thoracic vascular operations without CPB. Concentration of C3, as measured by radioimmunoassay, was used as an indicator of complement activation (C3a is a complement-degradation product). In the CPB patients, the C3a level increased tenfold (from baseline value) after the onset of bypass, and continued to increase during bypass. Protamine produced an additional twofold increase in the C3a value, to a peak of 5461 +/- 1360 ng/ml. By 12 hours after surgery, the C3a level had decreased to normal (400 ng/ml). In the non-CPB patients, C3a remained at baseline levels until the administration of protamine, which caused a tenfold increase to a peak of 2281 +/- 293 ng/ml; C3a levels returned to normal 6 hours after operation. The peak postprotamine C3a levels were significantly higher (p < 0.01) in the CPB group than in the non-CPB group. This finding was due to the fact that, during CPB, complement activation occurs via the alternative pathway; the administration of protamine then causes additional activation via the classical pathway. During thoracic vascular operations, however, complement activation occurs only in response to protamine, via the classical pathway.