Born G V
Arzneimittelforschung. 1981;31(11a):2012-4.
Blood platelets can initiate arterial thrombosis by aggregating on atheromatous lesions and by accelerating the intrinsic coagulation system. The conversion of unreactive to reactive platelets (platelet activation) may be due to contact with vessel wall collagen and/or haemodynamic abnormalities in narrowed arteries, increasing the physical and chemical interactions with erythrocytes. Platelet activation is difficult to demonstrate and quantify in vivo. Proposed parameters include appearance of procoagulant (platelet factor 3) activity and other platelet-derived aggregating agents, notably prostaglandin endoperoxides and thromboxanes; appearance of "spontaneous" aggregates in the blood; alterations in ultrastructure, e.e., fewer dense inclusion bodies indicating the release reaction; and appearance of other released materials, e.g., platelet factor 4 which neutralises heparin and beta-thromboglobulin, both measurable by radioimmunoassay. Investigations of the biomedical mechanisms underlying platelet activation has brought up inhibitors of their reactions to aggregating agents in vitro and in vivo. Increases in bleeding time caused by such agents indicate that one or other may, if otherwise acceptable, be effective therapeutically against platelet-dependent thromboses. The recent discovery of prostacyclin and its biological effects may explain some of the problems besetting the outcome and interpretation of clinical trials so far.
血小板可通过在动脉粥样硬化病变处聚集以及加速内源性凝血系统来引发动脉血栓形成。无反应性血小板向反应性血小板的转变（血小板活化）可能是由于与血管壁胶原接触和/或狭窄动脉中的血流动力学异常，从而增加了与红细胞的物理和化学相互作用。血小板活化在体内难以证实和量化。提出的参数包括促凝剂（血小板因子3）活性和其他血小板衍生的聚集剂的出现，特别是前列腺素内过氧化物和血栓素；血液中“自发”聚集体的出现；超微结构的改变，例如，致密包涵体减少表明发生了释放反应；以及其他释放物质的出现，例如可通过放射免疫测定法测量的中和肝素的血小板因子4和β-血栓球蛋白。对血小板活化潜在生物医学机制的研究已经发现了体外和体内抑制其对聚集剂反应的物质。此类物质导致出血时间延长表明，如果在其他方面可以接受，其中一种或另一种物质可能在治疗血小板依赖性血栓形成方面有效。最近对前列环素及其生物学效应的发现可能解释了迄今为止困扰临床试验结果和解释的一些问题。
