O'Grady J, Hedges A, Whittle B J, Al-Sinawi L A, Mekki Q A, Burke C, Moody S G, Moti M J, Hassan S
Br J Clin Pharmacol. 1984 Dec;18(6):921-33. doi: 10.1111/j.1365-2125.1984.tb02565.x.
The effects of 9 beta-methyl carbacyclin, a chemically stable analogue of epoprostenol (prostacyclin, PGI2) were studied, in comparison with epoprostenol, both in vitro and in vivo in man. In vitro 9 beta-methyl carbacyclin and epoprostenol inhibited platelet aggregation induced by ADP, collagen, the endoperoxide analogue U46619 and arachidonic acid. The potency of 9 beta-methyl carbacyclin relative to epoprostenol was comparable in ADP and collagen-aggregated platelet rich plasma (PRP), 9 beta-methyl carbacyclin being 0.01 times as active as epoprostenol. The anti-aggregatory potencies of the two compounds were comparable in PRP and whole blood. The phosphodiesterase inhibitor isobutyl methyl xanthine enhanced the anti-aggregatory activity of both compounds in vitro. 9 beta-methyl carbacyclin and epoprostenol elevated platelet cyclic AMP, 9 beta-methyl carbacyclin being 0.04 times as active as epoprostenol. In a placebo controlled trial both drugs produces significant headache and facial flushing when compared with placebo. Nasal stuffiness, abdominal discomfort and nausea were reported on all three treatments. Both drugs caused significant and comparable increase in heart rate and decrease in pre-ejection (PEP) and PEP/left ventricular ejection time (LVET) ratio compared with placebo. Systolic and diastolic blood pressure, LVET and QS2 index were unchanged. Platelet aggregation responses to ADP were significantly inhibited by all three doses of both drugs compared with placebo. Bleeding time was significantly longer during epoprostenol infusion than either placebo or 9 beta-methyl carbacyclin infusion. Neither drug had significant effect, compared with placebo, on kaolin activated clotting time in PPP, PRP or in PRP in the presence of heparin, prothrombin time, partial thromboplastin time, thrombin clotting time, fibrinogen, fibrinogen degradation products or euglobulin clot lysis time. The pharmacodynamic effects and duration of action of 9 beta-methyl carbacyclin and of epoprostenol are similar; 9 beta-methyl carbacyclin is approximately 100 times less potent than epoprostenol in man.
对9β-甲基卡巴前列素(依前列醇(前列环素,PGI2)的一种化学稳定类似物)的作用进行了研究,并与依前列醇进行比较,研究在人体外和体内进行。在体外,9β-甲基卡巴前列素和依前列醇抑制由二磷酸腺苷(ADP)、胶原、内过氧化物类似物U46619和花生四烯酸诱导的血小板聚集。在ADP和胶原聚集的富血小板血浆(PRP)中,9β-甲基卡巴前列素相对于依前列醇的效力相当,9β-甲基卡巴前列素的活性是依前列醇的0.01倍。两种化合物在PRP和全血中的抗聚集效力相当。磷酸二酯酶抑制剂异丁基甲基黄嘌呤在体外增强了两种化合物的抗聚集活性。9β-甲基卡巴前列素和依前列醇升高血小板环磷酸腺苷(cAMP),9β-甲基卡巴前列素的活性是依前列醇的0.04倍。在一项安慰剂对照试验中,与安慰剂相比,两种药物均产生明显的头痛和面部潮红。所有三种治疗均报告有鼻塞、腹部不适和恶心。与安慰剂相比,两种药物均导致心率显著且相当程度的增加,射血前期(PEP)和PEP/左心室射血时间(LVET)比值降低。收缩压和舒张压、LVET和QS2指数无变化。与安慰剂相比,两种药物的所有三个剂量均显著抑制对ADP的血小板聚集反应。依前列醇输注期间的出血时间显著长于安慰剂或9β-甲基卡巴前列素输注。与安慰剂相比,两种药物对PPP、PRP或存在肝素的PRP中的高岭土激活凝血时间、凝血酶原时间、部分凝血活酶时间、凝血酶凝血时间、纤维蛋白原、纤维蛋白原降解产物或优球蛋白凝块溶解时间均无显著影响。9β-甲基卡巴前列素和依前列醇的药效学作用和作用持续时间相似;在人体中,9β-甲基卡巴前列素的效力比依前列醇低约100倍。