作者: J Vermylen , H Deckmyn
DOI: 10.1111/J.1365-2125.1983.TB02102.X
关键词: Platelet 、 Internal medicine 、 Thromboxane receptor 、 Prostacyclin 、 Biology 、 Thromboxane 、 In vivo 、 Thromboxane-A synthase 、 Dazoxiben 、 Thromboxane A2 、 Endocrinology
摘要: 1 Work with dazoxiben in vitro and vivo suggests that a diminished capacity of platelets to synthesize thromboxane A2 results reorientation the metabolism cyclic endoperoxides. 2 Platelets patients congenital synthetase deficiency show same phenomenon. 3 In presence endothelium or leukocytes which have prostacyclin capacity, significant amounts can be generated if synthesis is blocked. 4 The local generation aggregation inhibiting prostaglandins areas vascular damage may an interesting therapeutic concept. 5 Pilot clinical studies inhibitor (UK 37248) small number peripheral arterial disease did not reveal major consistent haemodynamic changes. 6 Attention directed towards optimizing pharmacologically efficacy inhibitory produced when inhibited.