Hemostasis in Patients Undergoing Extracorporeal Circulation: The Effect of Aprotinin (Trasylol)
Autor: | Yves Legrand, Armand Piwnica, Jeannette Soria, Claudine Soria, Friedrich Schumann, Pierre-Louis Commin, Odile Regnier, He Lu, Jacques Philippe Caen |
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Rok vydání: | 1991 |
Předmět: | |
Zdroj: | Thrombosis and Haemostasis. 66:633-637 |
ISSN: | 2567-689X 0340-6245 |
DOI: | 10.1055/s-0038-1646477 |
Popis: | SummaryThe administration of aprotinin during extracorporeal circulation (ECC) reduces blood loss. To explore the mechanism of this effect, a placebo-controlled double-blind study was performed in 20 patients (10 were administered with a high dose of aprotinin, 10 with placebo) undergoing a primary, elective operation of coronary artery bypass grafting (CABG) with ECC. Biological tests were performed at 4 different time points during the operation.A marked reduction in the placebo group of ristocetin-induced platelet agglutination (binding of von Willebrand factor [vWF] to platelet glycoprotein [GP] Ib) was shown during ECC and at the end of surgery, but not in the aprotinin group. This abnormality is not related to the hydrolysis of vWF or GP Ib, since washed platelets were resuspended in pooled normal plasma which provided a constant amount of vWF in this test and since the plasma concentration of the fragment of GP Ib (glycocalicin) did not correlate with this abnormality.Despite a high concentration of heparin (5-7 IU/ml) in patient's plasma during bypass, activation of blood coagulation in both groups was evidenced by an increase in ATm (thrombin-modified antithrombin III) level. The level of ATm in the placebo group reached a maximum at the end of ECC during rewarming, while in the aprotinin group, ATm level at this time point was significantly lower than in the control group. In comparison to the placebo group, the generation of the fibrin degradation products (DDE complexes) was inhibited by aprotinin during ECC, but the level of DDE complexes in the aprotinin group was slightly elevated after ECC, although much less than in the placebo group. Other parameters measured did not show significant differences between the two groups.These results indicate that the hemostatic defect in patients during and after ECC may result, at least in part, from the impairment of GP Ib-dependent platelet adhesion. Therefore, the administration of aprotinin in ECC may improve hemostasis by abrogating this impairment, in addition to the protective effect of aprotinin on hemostatic plug. Activation of blood coagulation occurs during cardiopulmonary bypass despite heparin therapy and this activation seems to be partially inhibited by aprotinin administration. |
Databáze: | OpenAIRE |
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