De Clerck F
Department of Cardiovascular Pharmacology, Janssen Research Foundation, Beerse, Belgium.
Clin Physiol Biochem. 1990;8 Suppl 3:40-9.
Serotonin, a weak activator on its own, elicits strong platelet reactions (aggregation, arachidonate metabolization, release reaction) through amplification. Such amplification operates via 5-HT2-serotonergic receptors which are linked to the turnover of polyphosphoinositides and increases of intracellular [Ca2+]i concentrations as signal transducing systems. In experimental animals, selective blockade of 5-HT2-serotonergic receptors eliminates arterial thrombus formation over sites of endothelial injury in stenosed canine coronaries; in combination with a manipulation of TXA2, it prevents coronary thrombotic reocclusion after fibrinolysis with rt-PA, and inhibits drastic platelet activation, elicited by injections of collagen in vivo. These observations suggest that serotonergic amplification substantially contributes to the aggregation of platelets in damaged vessels and offers perspectives for an improved antithrombotic approach.
血清素自身是一种弱激活剂，通过放大作用引发强烈的血小板反应（聚集、花生四烯酸代谢、释放反应）。这种放大作用通过5-HT2 - 血清素能受体起作用，这些受体与多磷酸肌醇的周转以及细胞内[Ca2+]i浓度的增加相关联，作为信号转导系统。在实验动物中，选择性阻断5-HT2 - 血清素能受体可消除狭窄犬冠状动脉内皮损伤部位的动脉血栓形成；与对血栓素A2的处理相结合，可预防rt - PA纤维蛋白溶解后冠状动脉血栓再闭塞，并抑制体内注射胶原蛋白引发的剧烈血小板激活。这些观察结果表明，血清素能放大作用在受损血管中血小板聚集中起重要作用，并为改进抗血栓方法提供了前景。
