APROTININ EFFECT ON PLATELET-FUNCTION AND CLOTTING DURING CARDIOPULMONARY BYPASS

被引:26
作者
TABUCHI, N [1 ]
DEHAAN, J [1 ]
BOONSTRA, PW [1 ]
HUET, RCGG [1 ]
VANOEVEREN, W [1 ]
机构
[1] UNIV GRONINGEN HOSP,THORAXCTR,9713 EZ GRONINGEN,NETHERLANDS
关键词
APROTININ; HEMOSTASIS; PLATELET FUNCTION; EXTRINSIC CLOTTING PATHWAY;
D O I
10.1016/1010-7940(94)90098-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
A variety of studies have been performed on the preservation of hemostasis by aprotinin during cardiopulmonary bypass (CPB). It appears that the mechanism of aprotinin to preserve hemostasis can be interpreted in different ways. Our previous studies suggested that preservation of platelet glycoprotein lb (GpIb) antigen, and counteraction of heparin anticoagulation in the extrinsic clotting pathway might partly explain the preservative effect of aprotinin. A clinical study was therefore conducted to evaluate these effects during the use of low dose aprotinin. Improved agglutination by ristocetin (P < 0.05), and improved GpIb antigen expression (P < 0.05) during CPB showed better preserved platelet adhesive capacity in the aprotinin group than in the control group. Glycoprotein lb antigen expression and the agglutination capacity with ristocetin during CPB were closely related (P < 0.05). Platelet GpIIb/IIIa antigen and adenosine diphosphate (ADP) aggregation were not significantly different between the aprotinin and control groups. Aprotinin had no effect on the extrinsic clotting pathway in the blood, since the thromboplastin clotting time was similar in both groups. These results indicate that the protection of platelet adhesive capacity during CPB is a main function of aprotinin, whereas no evidence was collected for enhanced extrinsic clotting by aprotinin during CPB.
引用
收藏
页码:87 / 90
页数:4
相关论文
共 19 条
[1]  
Bidstrup B.P., Royston D., Sapsford R.N., Taylor K.M., Reduction in blood loss and blood use after cardiopulmonary bypass with high dose aprotinin (Trasylol), J Thorac Cardio- Vasc Surg, 97, pp. 364-372, (1989)
[2]  
Blauhut B., Gross C., Necek S., Doran J.E., Spath P., Lundsgaard-Hansen P., Effects of high dose aprotinin on blood loss, platelet function, fibrinolysis, complement, and renal function after cardiopulmonary bypass, J Thorac Cardiovasc Surg, 101, pp. 958-967, (1991)
[3]  
Carson S.D., Johnson D.R., Consecutive enzyme cascade: Complement activation at the cell surface triggers increased tissue factor activity, Blood, 76, pp. 361-367, (1990)
[4]  
Coller B.C., Peerschke E.L., Scudder L.E., Sullivan C.A., Studies with a murine monoclonal antibody that abolishes ristocetin-induced binding of von Willebrand factor to platelet, Blood, 61, pp. 99-110, (1983)
[5]  
De Smet A., Joen M., Oeveren W., Van R.K., Harder M.P., Eijsman L., Wildevuur C., Increased anticoagulation during cardiopulmonary bypass by aprotinin, J Thorac Cardiovasc Surg, 100, pp. 520-527, (1990)
[6]  
Edmunds L.H., Niewiarowski S., Colman R.W., Aprotinin. J Thorac Cardiovasc Surg, 101, pp. 1103-1104, (1991)
[7]  
Escolar G., Monteagudo J., Villamor N., Garrido M., Castillo R., Ordinas A., Ristocetin induces platelet aggregation, Br J Haematol, 69, pp. 379-386, (1988)
[8]  
Havel M., Teufelsbauer H., Knobl P., Dalmatiner R., Jaksch P., Zwolfer W., Muller M., Vukovich T., Effect of intraoperative aprotinin administration on postoperative bleeding in patients undergoing cardiopulmonary bypass operation, J Thorac Cardiovasc Surg, 101, pp. 968-972, (1991)
[9]  
Havel M.P., Griesmacher A., Weigel G., Owen A., Simon P., Muller M.M., Wolner E., Aprotinin decreases release of 6-keto-prostaglandin Fla and increases release of thromboxane B2 in cultured human umbilical vein endothelial cells, J Thorac Cardiovasc Surg, 104, pp. 654-658, (1992)
[10]  
Jenkins C., Meyer D., Dreyfus M.D., Larrieu M.J., Willebrand factor and ristocetin, Br J Haematol, 28, pp. 561-578, (1974)