Platelet function during cardiac surgery and cardiopulmonary bypass with low-dose aprotinin.
OBJECTIVE
To determine whether two low-dose regimens of aprotinin influence platelet function.


METHODS
Prospective, randomized, single-blinded trial.


METHODS
University teaching hospital performing 600 cardiac operations per year.


METHODS
Fifty-nine patients scheduled for cardiac surgery undergoing cardiopulmonary bypass (CPB) of expected duration of 60 minutes or more.


METHODS
Patients were randomized into three groups. Group C (control) included 21 patients who did not receive aprotinin. In group A2, 17 patients received 14,286 kallikrein inhibitor units (KIU)/kg (2 mg/kg) of aprotinin before surgery, followed by a continuous infusion of 7,143 KIU/kg/h (1 mg/kg/h) until the end of surgery. In group A4, 19 patients received 28,572 KIU/kg (4 mg/kg) of aprotinin before surgery, followed by the same infusion.


RESULTS
Postoperative bleeding and transfusion requirements were significantly less in group A4. Changes in platelet number and function were similar in the three groups. Platelet aggregation was assessed in four periods: before CPB (T1), post-CPB (T2), and 2 hours (T3) and 4 hours (T4) after CPB. Platelet aggregation induced by adenosine diphosphate, 1 and 2 micromol/L; ristocetin, 1 mg/mL; and arachadonic acid (AA), 1.4 mmol/L, decreased at T2 (p < 0.001) in all groups, and for the ristocetin and AA groups, remained at less than baseline values at T3 and T4. In five patients from each group, platelet receptors for glycoprotein IIb-IIIa (GPIIb-IIIa) and expression of platelet activation markers, guanosine monophosphate 140 (GMP-140) and lysosomal protein, were measured by flow cytometry before and after CPB. Modifications in the expression of GPIIb-IIIa were always modest and without statistical significance. Platelet activation markers, GMP-140 or lysosomal protein, nearly doubled from baseline to post-CPB only in the A4 group, whereas they remained stable in both other groups (statistically not significant).


CONCLUSIONS
The two regimens of aprotinin, both considered low dosage, did not exert a protective effect on platelet function. Neither dose produced changes in platelet GPIIb-IIIa or platelet activation markers. However, bleeding and transfusion needs were decreased.
Basora
M
M
Department of Anesthesiology, Hospital Clínic, University of Barcelona, Spain.
Gomar
C
C
Escolar
G
G
Pacheco
M
M
Fita
G
G
Rodriguez
E
E
Ordinas
A
A
D000244:Adenosine Diphosphate / Q000494:pharmacology; D007611:Aprotinin / Q000008:administration & dosage*; D016718:Arachidonic Acid / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects* / Q000502:physiology; D001803:Blood Transfusion; D006348:Cardiac Surgical Procedures; D002315:Cardiopulmonary Bypass; D005260:Female; D006490:Hemostatics / Q000008:administration & dosage*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000032:analysis; D015539:Platelet Activation; D010974:Platelet Aggregation / Q000187:drug effects; D010976:Platelet Count; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000032:analysis; D019106:Postoperative Hemorrhage / Q000517:prevention & control; D011446:Prospective Studies; D012310:Ristocetin / Q000494:pharmacology; D016037:Single-Blind Method
D006490:Hemostatics; D019007:P-Selectin; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D012310:Ristocetin; D016718:Arachidonic Acid; D000244:Adenosine Diphosphate; D007611:Aprotinin