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首页> 外文期刊>Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis >The platelet-related effects of tenecteplase versus alteplase versus reteplase.
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The platelet-related effects of tenecteplase versus alteplase versus reteplase.

机译：替奈普酶与阿替普酶与瑞替普酶的血小板相关作用。

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Clinical studies have investigated the combination of glycoprotein (GP) IIb/IIIa inhibitors and thrombolytic agents for acute myocardial infarction. However, thrombolytic agents alone may possess direct antiplatelet properties that could affect reperfusion. Blood from 11 patients with coronary disease and five healthy subjects was incubated for 30 min with tenecteplase (4, 12, and 24 microg/ml), alteplase (1, 4, and 10 microg/ml), reteplase (1, 5, and 10 microg/ml) or control buffer. Platelet aggregation induced by 1, 20 and 50 micromol/l adenosine diphosphate (ADP), the stimulated expression of GP IIb/IIIa and P-selectin, and plasma fibrinogen levels were determined. Platelet aggregation in patients was inhibited by medium and high concentrations of alteplase when induced by 1 micromol/l ADP [1.6 +/- 0.5%, P = 0.001 and 0.9 +/- 0.2%, P = 0.002 versus 8.3 +/- 1.6% (control)] and 20 micromol/l ADP [46.9 +/- 3.9%, P = 0.001 and 46.2 +/- 4.8%, P = 0.001 versus 65.7 +/- 2.7% (control)]. High concentration tenecteplase was associated with lower aggregation by 20 micromol/l ADP (58 +/- 2.1% versus control, P = 0.033). There were no changes in GP IIb/IIIa activation or P-selectin expression in patients or healthy subjects. Platelet aggregation (1 micromol/l ADP) in healthy subjects was inhibited only by high doses of alteplase (P = 0.001). Plasma fibrinogen levels were significantly decreased after treatment with reteplase at 1 microg/ml(1.53 +/- 0.21 versus 2.65 +/- 0.31, P = .009) and 5 microg/ml(1.55 +/- 0.16 versus 2.65 +/- 0.31, P = .005). Alteplase inhibits platelet aggregation more than tenecteplase and reteplase. The attenuation of platelet aggregation by alteplase is dissociated from the expression of activated GP IIb/IIIa and P-selectin, and by fibrinogen degradation. These results suggest that alteplase exerts its antiplatelet effect independent of GP IIb/IIIa and P-selectin expressions and fibrinogen degradation. These findings may be directly relevant to the effect of alteplase on reperfusion and to future studies using combined platelet inhibitors and thrombolytic therapy.
机译：临床研究已经研究了糖蛋白（GP）IIb / IIIa抑制剂和溶栓剂对急性心肌梗死的联合治疗。但是，单独的溶栓剂可能具有直接的抗血小板特性，可能会影响再灌注。将来自11名冠心病患者和5名健康受试者的血液与替奈普酶（4、12和24 microg / ml），阿替普酶（1、4和10 microg / ml），瑞替普酶（1、5和5）孵育30分钟10 microg / ml）或对照缓冲液。测定了1、20和50微摩尔/升的二磷酸腺苷（ADP）诱导的血小板聚集，GP IIb / IIIa和P-选择素的刺激表达以及血浆纤维蛋白原水平。当由1 micromol / l ADP诱导时，中度和高浓度的阿替普酶可抑制患者的血小板聚集[1.6 +/- 0.5％，P = 0.001和0.9 +/- 0.2％，P = 0.002对8.3 +/- 1.6％ （对照）]和20 micromol / l ADP [46.9 +/- 3.9％，P = 0.001和46.2 +/- 4.8％，P = 0.001对65.7 +/- 2.7％（对照）]。高浓度替奈普酶与较低的聚集度相关，降低了20微摩尔/升ADP（相对于对照组为58 +/- 2.1％，P = 0.033）。患者或健康受试者的GP IIb / IIIa激活或P-选择素表达没有变化。健康受试者的血小板聚集（1 µmol / l ADP）仅被高剂量的阿替普酶抑制（P = 0.001）。分别使用1 mg / ml（1.53 +/- 0.21与2.65 +/- 0.31，P = 0.009）和5 microg / ml（1.55 +/- 0.16与2.65 +/- 0.31）的瑞替普酶治疗后，血浆纤维蛋白原水平显着降低，P = .005）。阿替普酶比替奈普酶和瑞替普酶更能抑制血小板凝集。阿替普酶对血小板凝集的抑制作用与激活的GP IIb / IIIa和P-选择素的表达以及纤维蛋白原降解无关。这些结果表明，阿替普酶发挥其抗血小板作用，与GP IIb / IIIa和P-选择素的表达以及纤维蛋白原的降解无关。这些发现可能与阿替普酶对再灌注的作用以及与使用联合血小板抑制剂和溶栓治疗的未来研究直接相关。

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