title: Hemostasis in patients undergoing extracorporeal circulation: the effect of aprotinin (Trasylol).
abstract: The 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.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: INSERM U 150, Institut des Vaisseaux et du Sang (IVS), Département d'Anesthésiologie, Hôpital Lariboisière, Paris, France.
authors.forename: H
authors.initials: H
authors.lastname: Lu
authors.forename: C
authors.initials: C
authors.lastname: Soria
authors.forename: P L
authors.initials: PL
authors.lastname: Commin
authors.forename: J
authors.initials: J
authors.lastname: Soria
authors.forename: A
authors.initials: A
authors.lastname: Piwnica
authors.forename: F
authors.initials: F
authors.lastname: Schumann
authors.forename: O
authors.initials: O
authors.lastname: Regnier
authors.forename: Y
authors.initials: Y
authors.lastname: Legrand
authors.forename: J P
authors.initials: JP
authors.lastname: Caen
mesh_terms: D000990:Antithrombin III / Q000032:analysis; D007611:Aprotinin / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects; D004311:Double-Blind Method; D004797:Enzyme-Linked Immunosorbent Assay; D005112:Extracorporeal Circulation / Q000009:adverse effects*; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006487:Hemostasis / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000032:analysis; D019038:Platelet Glycoprotein GPIb-IX Complex; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D011446:Prospective Studies; D012310:Ristocetin; D010959:Tissue Plasminogen Activator / Q000032:analysis
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D010975:Platelet Aggregation Inhibitors; D019038:Platelet Glycoprotein GPIb-IX Complex; D010980:Platelet Membrane Glycoproteins; C036309:fibrin fragment D; C023592:glycocalicin; D012310:Ristocetin; D000990:Antithrombin III; D007611:Aprotinin; D010959:Tissue Plasminogen Activator