Institution of Clinical Science, Medical Faculty, Lund University, S-22185, Lund, Sweden.
Department of Anaesthesiology and Intensive Care, Skane University Hospital, S-22185, Lund, Sweden.
BMC Complement Med Ther. 2020 Jul 2;20(1):204. doi: 10.1186/s12906-020-02990-9.
Omega-3 and acetylsalicylic acid (ASA) are two widely used "over-the-counter" drugs. Previous research has shown multiple electrode aggregometry (MEA) can detect ASA and varying Omega-3 platelet inhibiting effects. Synergistic platelet inhibiting effects of ASA and Omega-3 have been found using other methods than MEA. The aim of this study was to investigate the antiplatelet effects of Omega-3, and ASA synergism with MEA.
Ten healthy male volunteers ingested Omega-3 (1260 mg/day) for 5 days. MEA was used to analyse platelet function before and after Omega-3 intake. Aggregation was initiated using three different agonists and measured as area under the curve (AUC): adenosine diphosphate (ADP), thrombin receptor activating peptide (TRAP) and arachidonic acid (ASPI). Two concentrations of ASA were dose titrated ex vivo to 2 out of 3 ASPI test cells in order to measure synergism between Omega-3 and ASA.
Following 5 days Omega-3 intake, ADP, TRAP and ASPI AUC did not change significantly. In vitro ASA before Omega-3 intake, reduced ASPI AUC < 30 U, indicating a strong platelet inhibiting effect. Below this AUC level, the 5 days Omega-3 intake increased ASPI-AUC with the ex vivo added low dose ASA (P = 0.02) and high dose ASA (P = 0.04).
No synergism between ASA and Omega-3 was found using the MEA ASPI test. The surprising increase in ASPI-AUC following Omega-3 intake and ex vivo ASA suggest that there are methodological issuses with the MEA ASPI test.
Trial registration ISRCTN78027929 . Registered 19 May 2015.
ω-3 脂肪酸和乙酰水杨酸(ASA)是两种广泛使用的“非处方”药物。先前的研究表明,多电极聚集仪(MEA)可检测 ASA 和不同的 ω-3 血小板抑制作用。使用 MEA 以外的其他方法发现 ASA 和 ω-3 具有协同的血小板抑制作用。本研究旨在使用 MEA 研究 ω-3 的抗血小板作用以及 ASA 与 ω-3 的协同作用。
10 名健康男性志愿者连续 5 天每天摄入 1260mg ω-3 脂肪酸。在摄入 ω-3 脂肪酸前后使用 MEA 分析血小板功能。使用三种不同的激动剂(二磷酸腺苷、血栓素受体激活肽和花生四烯酸)启动聚集,并测量曲线下面积(AUC):ADP、TRAP 和 ASPI。体外剂量滴定 2 种 ASA 浓度至 3 个 ASPI 测试细胞中的 2 个,以测量 ω-3 与 ASA 之间的协同作用。
连续 5 天摄入 ω-3 脂肪酸后,ADP、TRAP 和 ASPI AUC 无明显变化。在摄入 ω-3 脂肪酸之前,体外 ASA 降低了 ASPI AUC<30U,表明具有很强的血小板抑制作用。在此 AUC 水平以下,5 天的 ω-3 脂肪酸摄入增加了添加低剂量 ASA(P=0.02)和高剂量 ASA(P=0.04)的 ASPI-AUC。
使用 MEA ASPI 测试未发现 ASA 和 ω-3 之间存在协同作用。在摄入 ω-3 脂肪酸和体外 ASA 后,ASPI-AUC 的惊人增加表明 MEA ASPI 测试存在方法问题。
试验注册 ISRCTN78027929。于 2015 年 5 月 19 日注册。