Menys V C, Davies J A
Thromb Haemost. 1983 Apr 28;49(2):96-101.
Platelet adhesion to rabbit aortic subendothelium or collagen-coated glass was quantitated in a rotating probe device by uptake of radio-labelled platelets. Under conditions in which aspirin had no effect, dazoxiben, a selective inhibitor of thromboxane synthetase, reduced platelet adhesion to aortic subendothelium by about 40% but did not affect adhesion to collagen-coated glass. Pre-treatment of aortic segments with 15-HPETE, a selective inhibitor of PGI2-synthetase, abolished the inhibitory effect of dazoxiben on adhesion. Concentrations of 6-oxo-PGF1 alpha in the perfusate were raised in the presence of dazoxiben alone, and following addition of thrombin (10 units/ml) there was a 2--3 fold increase in concentration. Perfusion of damaged aorta with platelets labelled with (14C)-arachidonic acid in the presence of thrombin and dazoxiben resulted in the appearance of (14C)-labelled-6-oxo-PGF1 alpha. Inhibition of thromboxane synthetase limits platelet adhesion probably by promoting vascular synthesis of PGI2 from endoperoxides liberated from adherent platelets, which subsequently promotes detachment of cells from the surface.
通过放射性标记血小板的摄取，在旋转探针装置中对血小板与兔主动脉内皮下层或胶原包被玻璃的黏附进行定量。在阿司匹林无作用的条件下，血栓素合成酶的选择性抑制剂达唑氧苯使血小板与主动脉内皮下层的黏附减少约40%，但不影响与胶原包被玻璃的黏附。用前列环素合成酶的选择性抑制剂15-HPETE预处理主动脉段，消除了达唑氧苯对黏附的抑制作用。单独存在达唑氧苯时，灌注液中6-氧代-PGF1α的浓度升高，加入凝血酶（10单位/毫升）后浓度增加2至3倍。在凝血酶和达唑氧苯存在的情况下，用(14C)-花生四烯酸标记的血小板灌注受损主动脉，导致出现(14C)-标记的6-氧代-PGF1α。血栓素合成酶的抑制可能通过促进从黏附血小板释放的内过氧化物合成血管前列环素，从而限制血小板黏附，进而促进细胞从表面脱离。
