Martini Angela K, Rodriguez Cassandra M, Cap Andrew P, Martini Wenjun Z, Dubick Michael A
aRice University, Houston bU.S. Army Institute of Surgical Research, JBSA - Fort Sam Houston, Texas, USA.
Blood Coagul Fibrinolysis. 2014 Dec;25(8):831-7. doi: 10.1097/MBC.0000000000000162.
Acetaminophen (Ace) and meloxicam (Mel) are the two types of analgesic and antipyretic medications. This study investigated the dose responses of acetaminophen and meloxicam on platelet aggregation and coagulation function in human blood samples. Blood samples were collected from six healthy humans and processed to make platelet-adjusted (100 × 10 cells/μl) blood samples. Acetaminophen (Tylenol, Q-PAP, 100 mg/ml) was added at the doses of 0 μg/ml (control), 214 μg/ml (the standard dose, 1 ×), 4 ×, 8 ×, 10 ×, 12 ×, 16 ×, and 20 ×. Similarly, meloxicam (Metacam, 5 mg/ml) was added at doses of 0 μg/ml (control), 2.85 μg/ml (the standard dose, 1 ×), 4 ×, 8 ×, 10 ×, 12 ×, 16 ×, and 20 ×. Fifteen minutes after the addition of acetaminophen and/or meloxicam, platelet aggregation was stimulated with collagen (2 μg/ml) or arachidonic acid (0.5 mmol/l) and assessed using a Chrono-Log 700 aggregometer. Coagulation function was assessed by prothrombin time (PT), activated partial thromboplastin time (aPTT), and using Rotem thrombelastogram. A robust inhibition by acetaminophen and/or meloxicam was observed in arachidonic acid-stimulated platelet aggregation starting at 1 × dose. Collagen-stimulated platelet aggregation was inhibited by ACE starting at 1 × (78 ± 10% of control), and by meloxicam starting at 4 × (72 ± 5% of control, both P < 0.05). The inhibitions by acetaminophen and meloxicam combined were similar to those by acetaminophen or meloxicam. aPTT was prolonged by meloxicam starting at 4 ×. No changes were observed in PT or any of Rotem measurements by acetaminophen and/or meloxicam. Acetaminophen and meloxicam compromised platelet aggregation and aPTT. Further effort is warranted to characterize the effects of acetaminophen and meloxicam on bleeding in vivo.
对乙酰氨基酚（Ace）和美洛昔康（Mel）是两类解热镇痛药物。本研究调查了对乙酰氨基酚和美洛昔康对人血样本中血小板聚集和凝血功能的剂量反应。从6名健康人采集血样并进行处理，制成血小板调整后的（100×10⁹细胞/μl）血样。对乙酰氨基酚（泰诺林、Q - PAP，100mg/ml）以0μg/ml（对照）、214μg/ml（标准剂量，1×）、4×、8×、10×、12×、16×和20×的剂量添加。同样，美洛昔康（美达佳，5mg/ml）以0μg/ml（对照）、2.85μg/ml（标准剂量，1×）、4×、8×、10×、12×、16×和20×的剂量添加。添加对乙酰氨基酚和/或美洛昔康15分钟后，用胶原蛋白（2μg/ml）或花生四烯酸（0.5mmol/l）刺激血小板聚集，并使用Chrono - Log 700血小板聚集仪进行评估。通过凝血酶原时间（PT）、活化部分凝血活酶时间（aPTT）以及使用旋转血栓弹力图评估凝血功能。在花生四烯酸刺激的血小板聚集中，从1×剂量开始观察到对乙酰氨基酚和/或美洛昔康有显著抑制作用。胶原蛋白刺激的血小板聚集从1×剂量开始被对乙酰氨基酚抑制（为对照的78±10%），从4×剂量开始被美洛昔康抑制（为对照的72±5%，两者P<0.05）。对乙酰氨基酚和美洛昔康联合使用的抑制作用与对乙酰氨基酚或美洛昔康单独使用时相似。美洛昔康从4×剂量开始使aPTT延长。对乙酰氨基酚和/或美洛昔康未观察到PT或旋转血栓弹力图的任何测量值有变化。对乙酰氨基酚和美洛昔康损害血小板聚集和aPTT。有必要进一步研究对乙酰氨基酚和美洛昔康对体内出血的影响。
