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目的观察地奥心血康对阿司匹林抵抗患者的干预效果并探讨其作用机制。方法将60例阿司匹林抵抗患者随机分为加大阿司匹林用量组(对照组,拜阿司匹林300 mg/d)30例,地奥心血康组(治疗组,地奥心血康1.6 g,每日3次)30例。两组均连续用药4周。观察并对比血小板平均聚集率、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-K-PGF1α)及药物安全性。结果治疗组有效率显著高于对照组;治疗组治疗1个月后以花生四烯酸(AA)和二磷酸腺苷(ADP)诱导的血小板聚集率及其下降值均显著低于对照组。与治疗前比较,对照组和治疗组的TXB2均升高明显(P<0.01)。治疗组的6-K-PGF1α与对照组相比升高(P<0.05),与治疗前比较,对照组降低明显(P<0.01)。与治疗前比较,对照组和治疗组的TXB2/6-K-PGF1α均降低(P<0.01,P<0.05)。治疗组药物不良反应发生率显著低于对照组。结论地奥心血康治疗阿司匹林抵抗有较好的疗效及安全性,其机制可能与其可降低TXB2同时升高6-K-PGF1α,降低TXB2/6-K-PGF1α的作用有关。
Objective To observe the intervention effect of Dioxin Xingsangkang on patients with aspirin resistance and to explore its mechanism. Methods Sixty patients with aspirin resistance were randomly divided into three groups: 30 cases in aspirin group (control group, aspirin 300 mg / d) and 30 cases in Dioxintangxuekang group (treated group, Dioganxuankang 1.6 g, 3 times daily). Two groups were treated for 4 weeks. The average platelet aggregation rate, thromboxane B2 (TXB2), 6-keto-prostaglandin F1α (6-K-PGF1α) and drug safety were observed and compared. Results The effective rate of the treatment group was significantly higher than that of the control group. The platelet aggregation rate and its decline value induced by arachidonic acid (AA) and adenosine diphosphate (ADP) in the treatment group after 1 month were significantly lower than those in the control group. Compared with before treatment, TXB2 in control group and treatment group increased significantly (P <0.01). The 6-K-PGF1α in the treatment group was significantly higher than that in the control group (P <0.05), and the control group was significantly lower than that before treatment (P <0.01). Compared with those before treatment, TXB2 / 6-K-PGF1α in control group and treatment group decreased (P <0.01, P <0.05). The incidence of adverse drug reactions in the treatment group was significantly lower than that in the control group. CONCLUSION: Dioxin Xueshikang has good efficacy and safety in the treatment of aspirin resistance. Its mechanism may be related to the decrease of TXB2, simultaneous increase of 6-K-PGF1α and decrease of TXB2 / 6-K-PGF1α.