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首页> 外文期刊>Thrombosis Research: An International Journal on Vascular Obstruction, Hemorrhage and Hemostasis >The potential mechanism for the effect of heparin on tissue plasminogen activator-mediated plasminogen activation.
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The potential mechanism for the effect of heparin on tissue plasminogen activator-mediated plasminogen activation.

机译：肝素对组织纤溶酶原激活物介导的纤溶酶原激活作用的潜在机制。

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The effects and possible role of heparin on tissue plasminogen activator-mediated plasminogen activation was thoroughly investigated. Direct analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis demonstrated that heparin increased the conversion of plasminogen to plasmin. Experiments by fluorescence quenching suggested that the stimulation of tissue plasminogen activator activity probably was due to a direct binding of heparin to tissue plasminogen activator, causing a conformational change of tissue plasminogen activator and rendering it more accessible to plasminogen interaction. The absence of additive stimulation effects on tissue plasminogen activator-mediated plasminogen activation when both heparin and fibrinogen were present also implied that both compounds interacted with tissue plasminogen activator via the same domain; it appeared to be most likely via the kringle-2 domain in tissue plasminogen activator based on studies using epsilon-aminocaproic acid as an inhibitor. Unlike heparin-induced stimulation of antithrombin-thrombin interaction, the heparin-induced stimulation of tissue plasminogen activator did not seem to follow a template model. Only in the presence of a high plasminogen or a low tissue plasminogen activator concentration, massive stimulation of tissue plasminogen activator activity was observed via a pseudotemplate model. The results suggest that precautions concerning high heparin dose should be given during its conjunctive clinical use with tissue plasminogen activator in thrombolytic therapy to reduce the risk of hemorrhage.
机译：彻底研究了肝素对组织纤溶酶原激活物介导的纤溶酶原激活的影响及其可能的作用。通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳的直接分析表明，肝素增加了纤溶酶原向纤溶酶的转化。通过荧光猝灭的实验表明，刺激组织纤溶酶原激活物的活性可能是由于肝素与组织纤溶酶原激活物的直接结合，导致组织纤溶酶原激活物的构象变化，并使纤溶酶原相互作用更加容易。当肝素和纤维蛋白原同时存在时，对组织纤溶酶原激活物介导的纤溶酶原激活没有附加刺激作用，这也暗示这两种化合物都通过同一域与组织纤溶酶原激活物相互作用。根据使用ε-氨基己酸作为抑制剂的研究，它似乎最有可能是通过组织纤溶酶原激活剂中的kringle-2结构域形成的。与肝素诱导的抗凝血酶-凝血酶相互作用的刺激不同，肝素诱导的组织纤溶酶原激活物的刺激似乎没有遵循模板模型。仅在高纤溶酶原或低组织纤溶酶原激活物浓度存在下，才通过伪模板模型观察到组织纤溶酶原激活物活性的大量刺激。结果表明，在溶栓治疗中将肝素与组织纤溶酶原激活剂联合用于临床时，应注意预防高剂量肝素，以减少出血的风险。

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