Sakata T, Kobayashi K, Katayama Y, Takada T, Matsuyama T
Department of Clinical Laboratory, National Cardiovascular Center, Suita.
Rinsho Byori. 1991 Mar;39(3):315-20.
It is necessary in clinical to establish the effects of new substances for the primary and secondary prevention of thrombotic illnesses. We measured maximum aggregation after addition of collagen (F.C. 1.7 micrograms/ml) or ADP (F.C. 1.7 mumol/l) in 41 patients without drug treatment, 91 with ticlopidine, 22 with aspirin (ASA); 82-750 mg, 13 with ASA 81 mg, 20 with ticlopidine 100 mg and ASA 81 mg, 13 with cilostazol, 25 with flurbiprofen, 19 with nifedipine and evaluated the ex vivo effect of platelet antagonists. ASA inhibited remarkably collagen-induced platelet aggregation compared with other drugs, but there was significant (p less than 0.01 for 0.5 mumol/l ADP; p less than 0.02 for 1.0 mumol/l ADP) increase of primary aggregation induced by low dose of ADP in 14 healthy volunteers. While ticlopidine only significantly reduced ADP-induced platelet aggregation and we couldn't find dose dependency of ticlopidine (100-300 mg/day) on inhibitory effects of ADP or collagen-induced platelet aggregation. Our results indicate that the administration of one tablet of aspirin for pediatrics (aspirin 81 mg/tab) together with ticlopidine 100 mg is suitable for reduction of platelet aggregation.
临床上有必要确定新物质对血栓性疾病一级和二级预防的效果。我们在41例未接受药物治疗的患者、91例接受噻氯匹定治疗的患者、22例接受阿司匹林（ASA）治疗（82 - 750毫克）的患者、13例接受81毫克ASA治疗的患者、20例接受100毫克噻氯匹定和81毫克ASA治疗的患者、13例接受西洛他唑治疗的患者、25例接受氟比洛芬治疗的患者、19例接受硝苯地平治疗的患者中，加入胶原蛋白（终浓度1.7微克/毫升）或ADP（终浓度1.7微摩尔/升）后测量最大聚集率，并评估血小板拮抗剂的体外效应。与其他药物相比，ASA显著抑制胶原蛋白诱导的血小板聚集，但在14名健康志愿者中，低剂量ADP（0.5微摩尔/升时p < 0.01；1.0微摩尔/升时p < 0.02）诱导的初级聚集有显著增加。而噻氯匹定仅显著降低ADP诱导的血小板聚集，且我们未发现噻氯匹定（100 - 300毫克/天）对ADP或胶原蛋白诱导的血小板聚集抑制作用存在剂量依赖性。我们的结果表明，儿科服用一片阿司匹林（81毫克/片）联合100毫克噻氯匹定适合降低血小板聚集。
