Menys V C, Davies J A
Clin Sci (Lond). 1983 Aug;65(2):149-53. doi: 10.1042/cs0650149.
The effects of ZK 36374, a prostacyclin analogue, were studied on adhesion of rabbit platelets to damaged rabbit aorta and on activation of platelets (judged by release of serotonin and formation of thromboxane-B2) in response to the processes of adhesion to the vessel surface and aggregation in response to microfibrillar collagen in suspension. In the presence of ZK 36374 (10-100 nmol/l), platelet adhesion and thromboxane-B2 formation were progressively reduced. The extent of serotonin release from adherent platelets was similar to that found for platelets aggregated with collagen. However, higher concentrations of ZK 36374 were required to inhibit serotonin release from adherent platelets than from aggregated platelets. The results indicate that ZK 36374 acts similarly to native prostacyclin on adhesion and collagen-induced aggregation and unlike previously described analogues is equipotent. The mechanism of release of serotonin induced by adhesion of platelets is less sensitive to the action of ZK 36374 than that of release induced by aggregation in response to microfibrillar collagen in suspension.
研究了前列环素类似物ZK 36374对兔血小板与受损兔主动脉黏附的影响,以及对血小板活化(通过血清素释放和血栓素B2形成来判断)的影响,血小板活化是对血管表面黏附过程以及对悬浮微原纤维胶原聚集反应的响应。在存在ZK 36374(10 - 100 nmol/L)的情况下,血小板黏附和血栓素B2形成逐渐减少。从黏附血小板释放的血清素程度与用胶原聚集的血小板相似。然而,抑制黏附血小板释放血清素所需的ZK 36374浓度高于抑制聚集血小板释放血清素所需的浓度。结果表明,ZK 36374在黏附和胶原诱导的聚集方面的作用与天然前列环素相似,并且与先前描述的类似物不同,具有同等效力。血小板黏附诱导的血清素释放机制对ZK 36374作用的敏感性低于悬浮微原纤维胶原聚集诱导的释放机制。