Aprotinin restores the adhesive capacity of dysfunctional platelets

摘要: The post-operative coagulopathy associated with cardiopulmonary bypass (CPB) is known to be predominantly related platelet dysfunction. use of the serine protease inhibitor aprotinin dramatically reduces CPB hemorrhage and thought act primarily through inhibition plasmin without directly influencing platelets. Our data indicate that there a direct effect on adhesion, which has not been previously reported. We found when was added blood samples poorly adhesive platelets, adhesion significantly increased as measured by percent coverage denuded arterial segments in Baumgartner perfusion chamber. In preliminary experiments using expired concentrates or fresh whole blood, addition induced positive increase 22+/-7.5 14+/-6.2 percentage point respectively. A simulated model recirculated unit anticoagulated for 2 h used (n=14) induce defect similar seen clinical CPB. At initiation recirculation, 55+/-9.5% but dropped 13+6.5% after post-recirculation significant restoration back 38+/-11% coverage. When epsilon amino-caproic acid soybean trypsin post recirculation samples, no scores. To compare these findings surgical CPB, we collected one sample at beginning two end from each seven open-heart patients. Aprotinin post-CPB samples. Platelet onset only 39+/-11% this patient group 7+/-7% end. Similar model, restored 29+/-11%. These results suggest some action other than its antiplasmin effect, general can promoted aprotinin.