Cardiac operations using cardiopulmonary bypass (CPB) are associated with a systemic inflammatory response most likely attributable to the release of various inflammatory mediators and activation of complement or coagulation cascade. In addition, (circulating) adhesion molecules, such as endothelial leukocyte adhesion molecule (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1), appear to be of central importance in the CPB-related inflammatory process. In this situation, antiproteases, such as aprotinin, may help to prevent damage of endothelial integrity. In a prospective study, 40 consecutive patients undergoing elective cardiac operation were randomly divided into two groups (with 20 patients in each group): in group 1 ''high-dose'' aprotinin was used (2 million IU of aprotinin before CPB, 500,000 IU/h until end of operation, 2 million IU added to the prime) (with aprotinin), and in group 2 no aprotinin was given (without aprotinin). Circulating adhesion molecules (cICAM-1, cELAM-1, and cVCAM-1) were measured from arterial blood samples using ELISA after induction of anesthesia (baseline), during CPB, at the end of the operation, 5 hours after CPB, and on the first postoperative day. The two groups were comparable concerning their biometric profile and CPB data. Baseline values of circulating adhesion molecules were within normal range and similar in both groups. During CFB, hemodilution resulted in a decrease in all circulating adhesion molecules. On the first postoperative day, cICAM-1 (with aprotinin, 215 +/- 32 ng/mL; without aprotinin, 230 +/- 40 ng/mL) and cELAM-1 (with aprotinin, 28 +/- 6 ng/mL; without aprotinin, 31 +/- 6 ng/mL) returned to baseline values. Only cVCAM-1 plasma levels were increased beyond baseline values at this data point (with aprotinin, 576 +/- 41 ng/mL; without aprotinin, 588 +/- 31 ng/mL,) without exceeding normal range. None of the patients suffered from high fever (temperature more than 38.5 degrees C), organ dysfunction, or needed prolonged intensive care therapy. It can be concluded that circulating adhesion molecules cICAM-1, cELAM-1, and cVCAM-1 were not markedly changed in our patients undergoing elective cardiac operations, which indicates only a limited endothelial damage or inflammatory response, respectively. Proteinase inhibitor aprotinin did not influence plasma levels of circulating adhesion molecules in this situation.
