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凝血酶诱导的血小板与惰性颗粒的聚集。

Aggregation of platelets and inert particles induced by thrombin.

作者信息

Chao F C, Tullis J L, Conneely G S, Lawler J W

出版信息

Thromb Haemost. 1976 Jun 30;35(3):717-36.

PMID:10638
Abstract

Thrombin-induced platelet aggregation and release were investigated in washed platelet suspensions and in suspensions of inert particles in order to evaluate the role of fibrinogen-fibrin transformation in aggregometer tracings. Thrombin (0.25-2.0 U/ml) produced two waves of light transmission increase (LTI) in both platelet and inert particle suspensions containing fibrinogen, and concomittantly aggregates were observed under phase microscopy. Without fibrinogen, thrombin induced rapid release of platelet ADP but failed to cause second wave of LTI. The kinetics of LTI in platelet and inert particle systems were related to both thrombin and fibrinogen concentrations. A rapid second wave of LTI could be produced by direct interaction of thrombin-treated platelets or inert particles with polymerizing fibrin, and was inhibited by sodium sulfite and low pH of 5.1 which prevent fibrin monomer polymerization. No fibrin strands were noted in platelet aggregates fixed at the completion of the second wave of LTI. Apyrase and PGE1 inhibited the rate of first but not that of second wave LTI. The results suggest that the release of platelet ADP induced by thrombin primarily affects the first phase aggregation, and the second phase may result from interaction of thrombin-exposed platelets and polymerizing fibrin. Thus, the blood coagulation mechanism may be directly involved in platelet aggregation.

摘要

为了评估纤维蛋白原 - 纤维蛋白转化在凝聚仪描记图中的作用,在洗涤后的血小板悬浮液和惰性颗粒悬浮液中研究了凝血酶诱导的血小板聚集和释放。凝血酶(0.25 - 2.0 U/ml)在含有纤维蛋白原的血小板和惰性颗粒悬浮液中均产生两波透光率增加(LTI),并且在相差显微镜下观察到聚集物。在没有纤维蛋白原的情况下,凝血酶诱导血小板ADP快速释放,但未能引起第二波LTI。血小板和惰性颗粒系统中LTI的动力学与凝血酶和纤维蛋白原浓度均有关。凝血酶处理的血小板或惰性颗粒与聚合纤维蛋白的直接相互作用可产生快速的第二波LTI,并且被亚硫酸钠和5.1的低pH值抑制,这会阻止纤维蛋白单体聚合。在第二波LTI完成时固定的血小板聚集体中未观察到纤维蛋白链。腺苷三磷酸双磷酸酶和前列腺素E1抑制第一波LTI的速率,但不抑制第二波LTI的速率。结果表明,凝血酶诱导的血小板ADP释放主要影响第一阶段聚集,第二阶段可能是由暴露于凝血酶的血小板与聚合纤维蛋白的相互作用导致的。因此,血液凝固机制可能直接参与血小板聚集。

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