de Gaetano G, Remuzzi G, Mysliwiec M, Donati M B
Haemostasis. 1979;8(3-5):300-11. doi: 10.1159/000214320.
In several experimental and clinical conditions associated with thrombotic tendency, or complicated by thrombotic episodes, either prostacyclin (which inhibits platelet aggregation) or plasminogen activator (which promotes fibrinolysis), or both, appear to be decreased in the vessel wall. In other conditions, however, either activity may not change or even be increased. Possibly, vascular damage is followed by an early stimulation of both activities (a defence mechanism?) which may be subsequently reduced or exhausted. While the role of vascular plasminogen activator in haemorrhagic conditions is apparently unknown, prostacyclin activity appears to be markedly enhanced both in experimental animals and in patients with uraemia and bleeding complications. There is a suggestive evidence that uraemic plasma powerfully stimulates vascular prostacyclin generation.
在一些与血栓形成倾向相关或并发血栓形成事件的实验和临床情况下，血管壁中前列环素（抑制血小板聚集）或纤溶酶原激活剂（促进纤维蛋白溶解），或两者似乎都减少。然而，在其他情况下，任何一种活性可能不变甚至增加。可能血管损伤后会早期刺激这两种活性（一种防御机制？），随后可能会降低或耗尽。虽然血管纤溶酶原激活剂在出血性疾病中的作用显然尚不清楚，但在实验动物以及患有尿毒症和出血并发症的患者中，前列环素活性似乎明显增强。有提示性证据表明，尿毒症血浆能有力地刺激血管前列环素的生成。
