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组织型纤溶酶原激活剂和纤维蛋白单体在体外循环后回输 shed blood 期间协同导致血小板功能障碍。 (注:shed blood 这里可能表述有误,不太明确准确意思,可根据实际情况修正)

Tissue-type plasminogen activator and fibrin monomers synergistically cause platelet dysfunction during retransfusion of shed blood after cardiopulmonary bypass.

作者信息

de Haan J, Schönberger J, Haan J, van Oeveren W, Eijgelaar A

机构信息

Department of Cardiopulmonary Surgery, University Hospital Groningen, The Netherlands.

出版信息

J Thorac Cardiovasc Surg. 1993 Dec;106(6):1017-23.

PMID:8246533
Abstract

Reduced hemostasis and bleeding tendency after cardiopulmonary bypass results from platelet dysfunction induced by the bypass procedure. The causes of this acquired platelet dysfunction are still subject to discussion, although, recently, greater emphasis has been placed on an overstimulated fibrinolytic system as a probable cause. In the first part of this study we assessed the effects of postoperative retransfusion of shed blood on blood loss to patients undergoing cardiopulmonary bypass. We observed that increasing concentrations of fibrinogen degradation products and tissue-type plasminogen activator stimulating activity in shed blood correlated significantly with a higher postoperative bleeding tendency (p < 0.05 for both). We further noted that retransfusion of shed blood increased the total postoperative blood loss by 43% (925 versus 1320 ml, p < 0.05). On the basis of these clinical observations, we hypothesized that the increased bleeding tendency was caused by fibrinolysis. In the second part of this study we collected evidence in support of this hypothesis by an in vitro study, in which we introduced similar (pro)fibrinolytic activity to platelet-rich plasma and measured the influence of this treatment on platelet function indicated by ristocetin agglutination. Tissue-type plasminogen activator and fibrin monomers (tissue-type plasminogen activator stimulator) together induced severe platelet damage, resulting in a decreased ristocetin agglutination response. Therefore, we propose a fibrinolysis-related mechanism for platelet dysfunction during cardiopulmonary bypass, dependent on fibrinolytic factors such as fibrin monomers, D-dimers, and tissue-type plasminogen activator.

摘要

体外循环后止血功能降低和出血倾向是由体外循环手术诱导的血小板功能障碍所致。尽管最近人们更加强调过度激活的纤溶系统可能是导致这种获得性血小板功能障碍的原因,但该病因仍存在争议。在本研究的第一部分,我们评估了术后回输引流血对接受体外循环手术患者失血的影响。我们观察到,引流血中纤维蛋白原降解产物浓度的增加以及组织型纤溶酶原激活物刺激活性与术后较高的出血倾向显著相关(两者p均<0.05)。我们还进一步注意到,回输引流血使术后总失血量增加了43%(925毫升对1320毫升,p<0.05)。基于这些临床观察结果,我们推测出血倾向增加是由纤维蛋白溶解引起的。在本研究的第二部分,我们通过一项体外研究收集了支持这一假设的证据,在该研究中,我们向富含血小板的血浆中引入了类似的(促)纤溶活性,并测量了这种处理对用瑞斯托菌素凝集表示的血小板功能的影响。组织型纤溶酶原激活物和纤维蛋白单体(组织型纤溶酶原激活物刺激剂)共同导致严重的血小板损伤,从而使瑞斯托菌素凝集反应降低。因此,我们提出了一种与纤维蛋白溶解相关的机制,用于解释体外循环期间的血小板功能障碍,该机制依赖于纤维蛋白单体、D-二聚体和组织型纤溶酶原激活物等纤维蛋白溶解因子。

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