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在冠状动脉血栓溶解期间,用组织型等离子体激活剂进行血小板和血管功能
D M Kerins1, L Roy, G A FitzGerald
1Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37232.
Circulation
|December 1, 1989
概括
在冠状动脉血栓溶解过程中,血小板激活增加,使用组织型等离子体激活剂 (t-PA). 阿司匹林阻止了这一点,并且在再注射患者中减少的前环素 (PGI2) 可能表明血管损伤.
科学领域:
- 心血管医学 心血管医学
- 血液学 血液学 血液学
- 药理学 药理学是指药理学的学科.
背景情况:
- 血小板激活是血栓形成的关键因素,可能会阻碍血栓治疗的有效性.
- 组织型等离子素激活剂 (t-PA) 是急性心肌梗塞的关键治疗方法,但其疗效可能受到血小板反应的影响.
研究的目的:
- 在患有急性心肌梗塞的患者中,用静脉t-PA对冠状动脉血栓溶解期间的血小板激活进行研究.
- 评估血小板激活和再输血的标记物,以评估血小板甲2和前环素 (PGI2) 生物合成.
主要方法:
- 在接受t-PA治疗的患者中测量尿中的2,3-dinor-thromboxane B2和2,3-dinor-6-keto-PGF1α分泌量.
- 用阿司匹林预先治疗的患者与没有阿司匹林的患者中的代谢物水平的比较.
- 与再输血状态相关的代谢物水平的分析.
主要成果:
- 静脉注射t-PA显著增加了血栓素A2生物合成,通过尿液中的2,3-dinor-thromboxane B2水平在48小时内升高而表明.
- 阿司匹林治疗前取消了t-PA诱导的血素A2生物合成的增加.
- 前环素 (PGI2) 生物合成也在t-PA后增加,但这种增加在实现再输血的患者中明显较低,而不是那些没有实现再输血的患者.
结论:
- 这些发现提供了在t-PA介导的冠状动脉血栓溶解期间显著血小板激活的证据.
- 在成功再输血的患者中,PGI2生物合成的减少可能作为血管再输血损伤的标志物.
- 放大血小板激活可能是反损伤的结果,可能会影响治疗结果.
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