Deutsch E, Mörz R
Arzneimittelforschung. 1982;32(4):388-93.
The action of 3-[4,5-bis-(4-chlorophenyl)-oxazolyl-(2)-thio]-propionic acid (tioxaprofen, EMD 26 644), a non-steroidal antiinflammatory substance, on platelet function has been studied in vitro and ex vitro. Collagen-induced aggregation and the second phase of adrenaline-induced aggregation are inhibited by small concentrations of tioxaprofen, The ADP-induced aggregation being inhibited only by higher concentrations. The generation of malonedialdehyde (MDA) is blocked. The pathological spontaneous aggregation found by the method of Born was reversed after treatment, and the pathologically increased aggregation according to platelet aggregation test (PAT I) of Breddin was normalized. Tioxaprofen blocks the formation of thromboxane most probably by inhibition of cyclo-oxygenase, but an inhibition of thromboxane synthetase cannot be excluded by our results. The in vivo action starts immediately after ingestion of tioxaprofen and is maintained by small doses. By checking the routine parameters of the blood a slight increase of creatinine and blood urea nitrogen (BUN) and a slight reduction of gamma-GT and alkaline phosphatase were found, all values remaining within the reference interval.
非甾体类抗炎物质3-[4,5-双-(4-氯苯基)-恶唑基-(2)-硫代]-丙酸(替诺昔康,EMD 26 644)对血小板功能的作用已在体外和离体条件下进行了研究。低浓度的替诺昔康可抑制胶原蛋白诱导的聚集以及肾上腺素诱导聚集的第二阶段,而较高浓度时才抑制ADP诱导的聚集。丙二醛(MDA)的生成被阻断。经治疗后,采用博恩方法发现的病理性自发聚集得到逆转,布雷丁血小板聚集试验(PAT I)中病理性增加的聚集恢复正常。替诺昔康很可能通过抑制环氧化酶来阻断血栓素的形成,但我们的结果不能排除对血栓素合成酶的抑制作用。替诺昔康的体内作用在摄入后立即开始,并可通过小剂量维持。检查血液常规参数发现肌酐和血尿素氮(BUN)略有升高,γ-谷氨酰转移酶和碱性磷酸酶略有降低,所有数值均保持在参考区间内。