Smith I L, Martin T J
Haemostasis. 1982;11(2):119-27. doi: 10.1159/000214650.
A group of patients with myeloproliferative disorders was studies with respect to platelet aggregation responses, release of beta-thromboglobulin and incorporated 5-hydroxy-tryptamine, and synthesis of thromboxane b 2. In all patients the resting plasma beta-thrombo-globulin was elevated. Aggregation responses were frequently impaired to adrenaline, arachidonic acid, A23187 and the prostaglandin endoperoxide analogue, U44069. Both 5-hydroxy-tryptamine and beta-thromboglobulin release were greater with patients' platelets than with those of controls in response to adrenaline, ADP and U44069. The patients' platelets produced more thromboxane B2 than did controls, irrespective of the agonist used, yet those aggregating agents which are thought to act by generating thromboxane A2 were relatively ineffective in causing aggregation. This might reflect resistance to thromboxane A2 action in these patients, which is met by increased thromboxane formation.
对一组骨髓增殖性疾病患者进行了血小板聚集反应、β-血小板球蛋白释放、5-羟色胺摄取以及血栓素B2合成方面的研究。所有患者静息血浆β-血小板球蛋白均升高。对肾上腺素、花生四烯酸、A23187以及前列腺素内过氧化物类似物U44069的聚集反应常常受损。在对肾上腺素、二磷酸腺苷（ADP）和U44069的反应中，患者血小板释放的5-羟色胺和β-血小板球蛋白均多于对照组血小板。无论使用何种激动剂，患者血小板产生的血栓素B2均多于对照组，但那些被认为通过生成血栓素A2起作用的聚集剂在引起聚集方面相对无效。这可能反映了这些患者对血栓素A2作用的抵抗，这种抵抗通过增加血栓素的形成来应对。
