Hamazaki T, Fischer S, Schweer H, Meese C O, Urakaze M, Yokoyama A, Yano S
First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Biochem Biophys Res Commun. 1988 Mar 30;151(3):1386-94. doi: 10.1016/s0006-291x(88)80516-3.
Thirty ml of an emulsion containing 3 g of trieicosapentaenoyl-glycerol (90% pure, containing 5% arachidonic acid (AA)) was infused intravenously in 2 male healthy volunteers. Urine samples were collected for 24 h before and 48 h after the infusion in 5 periods. Urinary metabolites of prostaglandin (PG) I2/3 and thromboxane (TX) A2/3 (PGI2/3-M and TXB2/3-M, respectively) were extracted from the urinary samples and measured by GC-MS. Excretion of PGI3-M was markedly enhanced right after the infusion. Because PGI3 was produced without involvement of intestinal absorption of eicosapentaenoic acid (EPA), enhanced PGI3 formation was strongly suggested to take place in the vasculature. From the marked increment in TXB2/3-M after the infusion it was calculated that conversion rate of EPA to TXA3 was 8% of that of AA to TXA2 in this in vivo condition.
将30毫升含有3克三二十碳五烯酰甘油(90%纯,含5%花生四烯酸(AA))的乳剂静脉输注给2名健康男性志愿者。在输注前24小时和输注后48小时分5个时间段收集尿液样本。从尿液样本中提取前列腺素(PG)I2/3和血栓素(TX)A2/3的尿代谢物(分别为PGI2/3-M和TXB2/3-M),并通过气相色谱-质谱联用仪进行测量。输注后PGI3-M的排泄明显增强。由于PGI3的产生不涉及二十碳五烯酸(EPA)的肠道吸收,强烈提示增强的PGI3形成发生在脉管系统中。根据输注后TXB2/3-M的显著增加计算出,在这种体内条件下,EPA向TXA3的转化率是AA向TXA2转化率的8%。