Wu K K, Papp A C, Manner C E, Hall E R
J Clin Invest. 1987 Jun;79(6):1601-6. doi: 10.1172/JCI112995.
To test the hypothesis that prostacyclin (PGI2) is formed via a biochemical interaction between platelets and lymphocytes, we measured eicosanoids by high performance liquid chromatography (HPLC) and radioimmunoassay (RIA). A distinct 6-keto-prostaglandin F1 alpha (6KPGF1 alpha) peak was noted when [14C]arachidonic acid ([14C]AA) was added to the mixed cell preparations which was increased by pretreating platelets with 1-benzylimidazole (1-BI). Lymphocytes prelabeled with [14C]AA failed to form 6KPGF1 alpha when stimulated with phytohemagglutinin (PHA) or ionophore A23187. When the prelabeled platelets were suspended together with aspirin-treated lymphocytes and stimulated with ionophore, thrombin, or collagen, a 6KPGF1 alpha peak was detected and enhanced by 1-BI. These results were supported by quantifying the 6KPGF1 alpha content in the HPLC-purified fraction by RIA. Adding prostaglandin H2 (PGH2) directly to lymphocytes led to 6KPGF1 alpha production. Platelet aggregation and release were inhibited by lymphocytes in a dose-related manner. We conclude that lymphocytes possess PGI2 synthase activity which is capable of converting platelet-derived PGH2 into PGI2. PGI2 formed is sufficient to inhibit platelet function.
为了验证前列环素（PGI2）是通过血小板与淋巴细胞之间的生化相互作用形成的这一假设，我们采用高效液相色谱法（HPLC）和放射免疫分析法（RIA）对类花生酸进行了测定。当向混合细胞制剂中添加[14C]花生四烯酸（[14C]AA）时，观察到一个明显的6-酮-前列腺素F1α（6KPGF1α）峰，用1-苄基咪唑（1-BI）预处理血小板可使其增加。用[14C]AA预标记的淋巴细胞在用植物血凝素（PHA）或离子载体A23187刺激时未能形成6KPGF1α。当将预标记的血小板与经阿司匹林处理的淋巴细胞一起悬浮并用离子载体、凝血酶或胶原刺激时，检测到一个6KPGF1α峰，且1-BI可使其增强。通过RIA对HPLC纯化组分中的6KPGF1α含量进行定量，支持了这些结果。直接向淋巴细胞中添加前列腺素H2（PGH2）可导致6KPGF1α的产生。淋巴细胞以剂量相关的方式抑制血小板聚集和释放。我们得出结论，淋巴细胞具有PGI2合酶活性，能够将血小板衍生的PGH2转化为PGI2。形成的PGI2足以抑制血小板功能。
