Menter D G, Onoda J M, Moilanen D, Sloane B F, Taylor J D, Honn K V
J Natl Cancer Inst. 1987 May;78(5):961-9.
Prostacyclin was examined for its inhibitory effects on the tumor cell-induced platelet release reaction. Prostacyclin inhibited in a dose-dependent manner tumor cell-induced release of platelet dense granules and alpha-granules concomitant with an inhibition of platelet aggregation. Release was determined by assay of biochemical markers (serotonin for dense granules and beta-thromboglobulin for alpha-granules). A tenfold higher concentration of prostacyclin was required to inhibit completely serotonin release as compared to the concentration required for beta-thromboglobulin release. Correlative ultrastructural studies demonstrated that prostacyclin at doses of over 10 ng/ml inhibited the ultrastructural changes associated with tumor cell-induced platelet shape change and platelet granule release. Platelet aggregates exhibited the retention of granule reservoirs that could potentially be involved in long-term release of biologically active substances.
研究了前列环素对肿瘤细胞诱导的血小板释放反应的抑制作用。前列环素以剂量依赖的方式抑制肿瘤细胞诱导的血小板致密颗粒和α颗粒的释放，同时抑制血小板聚集。通过检测生化标志物（致密颗粒的血清素和α颗粒的β-血小板球蛋白）来确定释放情况。与抑制β-血小板球蛋白释放所需的浓度相比，完全抑制血清素释放所需的前列环素浓度要高十倍。相关的超微结构研究表明，剂量超过10 ng/ml的前列环素可抑制与肿瘤细胞诱导的血小板形状改变和血小板颗粒释放相关的超微结构变化。血小板聚集体显示出颗粒储存库的保留，这可能与生物活性物质的长期释放有关。
