Béguin S, Lindhout T, Hemker H C
Department of Biochemistry, University of Limburg, Maastricht, The Netherlands.
Thromb Haemost. 1989 Feb 28;61(1):25-9.
Amounts of human brain thromboplastin that do not stimulate thrombin generation in platelet poor plasma, were shown to advance by about 4 min an explosive formation of thrombin that occurs after recalcification in the presence of blood platelets. This synergistic effect is inhibited by the specific thrombin inhibitor hirudin and mimicked by adding low concentrations (less than 5 nM) of thrombin to platelet rich plasma. It is our conclusion that small amounts of thrombin, generated under the influence of thromboplastin induced procoagulant activity in the blood platelets. This activity is most likely mainly due to procoagulant phospholipids. Heparin inhibits this effect and retards the explosive thrombin formation. It does not, however, diminish the peak amount of thrombin eventually formed, because heparin neutralizing material released from the activated platelets quenches the heparin effect.
在缺乏血小板的血浆中不能刺激凝血酶生成的人脑凝血活酶量，被证明可使在血小板存在下重新钙化后发生的凝血酶爆发性形成提前约4分钟。这种协同效应被特异性凝血酶抑制剂水蛭素抑制，并通过向富含血小板的血浆中添加低浓度（小于5 nM）的凝血酶来模拟。我们的结论是，在凝血活酶诱导的血小板促凝活性影响下产生少量凝血酶。这种活性很可能主要归因于促凝磷脂。肝素抑制这种效应并延缓凝血酶的爆发性形成。然而，它并不会减少最终形成的凝血酶的峰值量，因为从活化血小板释放的肝素中和物质会消除肝素的作用。
