首页> 美国卫生研究院文献>The Journal of Clinical Investigation >Fibrinopeptide A cleavage and platelet release in whole blood in vitro. Effects of stimuli inhibitors and agitation.
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Fibrinopeptide A cleavage and platelet release in whole blood in vitro. Effects of stimuli inhibitors and agitation.

机译:体外全血中纤维蛋白肽A的裂解和血小板释放。刺激抑制剂和躁动的影响。

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摘要

The relationship between platelet release and fibrinopeptide A cleavage from fibrinogen to form fibrin I in vitro was examined in blood allowed to clot undisturbed or with gentle agitation. In undisturbed or agitated blood platelet release and fibrin I formation occurred simultaneously. When hirudin was added to undisturbed blood it prevented platelet release as well as fibrin I formation. In contrast, hirudin added to agitated blood had little effect on platelet release despite complete inhibition of fibrin I formation. Collagen added to either undisturbed or agitated blood increased platelet release and then fibrin I formation, and ADP added to undisturbed blood caused an initial burst of platelet release followed by slight acceleration of fibrinopeptide A cleavage. Prostaglandin E1 and theophylline prevented platelet release in both undisturbed and agitated blood, but did not affect fibrin I formation. The results with inhibitors in agitated blood suggest that fibrin I formation and platelet release can occur independently in the presence of the increased interactions induced by agitation. Addition of thrombin or tissue thromboplastin to undisturbed blood accelerated fibrin I formation with little effect on platelet release. Finally, initial thrombin formation in undisturbed blood appeared to be associated with the platelet surface. These relationships suggest that thrombin formation via the intrinsic system leads to thrombin generation on the platelet surface and simultaneous platelet release and fibrin I formation, while thrombin generated via tissue thromboplastin leads to thrombin formation in the plasma and fibrin I formation preceding platelet release. Activation by interaction of blood with collagen causes initial acceleration of platelet release and later acceleration of fibrin I formation.
机译:在允许凝血不受干扰或轻微搅动的血液中,检查了血小板释放与纤维蛋白肽A在体外从纤维蛋白原切割形成纤维蛋白I的关系。在不受干扰或激动的情况下,血小板释放和纤维蛋白I的形成同时发生。当将水rud素添加到不受干扰的血液中时,它会阻止血小板释放以及血纤蛋白I的形成。相比之下,尽管完全抑制了血纤维蛋白I的形成,但是在搅动的血液中加入水rud素对血小板释放的影响很小。添加到未扰动或搅动的血液中的胶原蛋白会增加血小板释放,然后形成血纤蛋白I,而添加到未扰动的血液中的ADP会导致血小板释放的最初爆发,然后轻微加速纤维蛋白肽A的裂解。前列腺素E1和茶碱可在不受干扰的血液和搅动的血液中阻止血小板释放,但不会影响纤维蛋白I的形成。激动性血液中抑制剂的结果表明,在搅拌引起的相互作用增加的情况下,纤维蛋白I的形成和血小板的释放可以独立发生。在不受干扰的血液中添加凝血酶或组织凝血活酶可加速纤维蛋白I的形成,而对血小板释放的影响很小。最后,在不受干扰的血液中最初的凝血酶形成似乎与血小板表面有关。这些关系表明,通过内在系统形成的凝血酶导致血小板表面上的凝血酶生成以及同时的血小板释放和纤维蛋白I的形成,而通过组织凝血活酶生成的凝血酶导致血浆中的凝血酶形成和血小板释放前的纤维蛋白I的形成。血液与胶原蛋白相互作用引起的激活会导致血小板释放的最初加速,然后加速纤维蛋白I的形成。

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