| MECHANISM OF PRESERVING EFFECT OF APROTININ ON PLATELET FUNCTION DURING CARDIOPULMONARY BYPASS |
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| 作者姓名： | 黄惠民 丁文祥 苏肇伉 张伟忠 |
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| 作者单位： | Department of Pediatric Cardiothoracic Surgery，Xinhua Hospital，SSMU，Shanghai，Department of Pediatric Cardiothoracic Surgery，Xinhua Hospital，SSMU，Shanghai，Department of Pediatric Cardiothoracic Surgery，Xinhua Hospital，SSMU，Shanghai，Department of Pediatric Cardiothoracic Surgery，Xinhua Hospital，SSMU，Shanghai |
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| 摘 要： | The deficiency of platelet function is the main defect of hemostatic mechanism during cardiopulmonary bypass (CPB), which attributed to the postoperative bleeding complication to a great extent. The proteinase inhibitor aprotinin was reported to have preserving effect on platelet adhesion during CPB. In this clinical reserch we found that CPB caused plasma alpha 2-antiplasmin decreasing, indicating the fibrinolytic system activation. Meanwhile, the ristocetin-induced aggregation declined to 39.6% and platelet GPIb decreased to 50% of preoperative value. However, by treatment with aprotinin, the plasma alpha 2-antiplasmin during CPB did not change, platelet aggregation was improved and platelet GPIb was preserved, and consequently resulted in a 46% lower blood loss postoperatively. These results confirmed that aprotinin could inhibit the fibrinolysis during CPB, and thus relieve the platelet damage and improve the postoperative hemostatic mechanism.
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MECHANISM OF PRESERVING EFFECT OF APROTININ ON PLATELET FUNCTION DURING CARDIOPULMONARY BYPASS |
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| Huang Huiming,Din Wenxiang,Su Zhaokang Zhang Weizhong.MECHANISM OF PRESERVING EFFECT OF APROTININ ON PLATELET FUNCTION DURING CARDIOPULMONARY BYPASS[J].Journal of Shanghai Second Medical University(Foreign Language Edition),1992(2). |
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| Authors: | Huang Huiming Din Wenxiang Su Zhaokang Zhang Weizhong |
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| Institution: | Huang Huiming,Din Wenxiang,Su Zhaokang Zhang Weizhong Department of Pediatric Cardiothoracic Surgery,Xinhua Hospital,SSMU,Shanghai |
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| Abstract: | The deficiency of platelet function is the main defect of hemostatic mechanism during cardiopulmonary bypass (CPB), which attributed to the postoperative bleeding complication to a great extent. The proteinase inhibitor aprotinin was reported to have preserving effect on platelet adhesion during CPB. In this clinical reserch we found that CPB caused plasma alpha 2-antiplasmin decreasing, indicating the fibrinolytic system activation. Meanwhile, the ristocetin-induced aggregation declined to 39.6% and platelet GPIb decreased to 50% of preoperative value. However, by treatment with aprotinin, the plasma alpha 2-antiplasmin during CPB did not change, platelet aggregation was improved and platelet GPIb was preserved, and consequently resulted in a 46% lower blood loss postoperatively. These results confirmed that aprotinin could inhibit the fibrinolysis during CPB, and thus relieve the platelet damage and improve the postoperative hemostatic mechanism. |
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| Keywords: | cardiopulmonary bypass aprotinin fibrinolytic system platelet membrane glycoprotein platelet adhesion |
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