Ginsberg M H, Kozin F, O'Malley M, McCarty D J
J Clin Invest. 1977 Nov;60(5):999-1007. doi: 10.1172/JCI108880.
The release of human platelet constituents by the etiologic agent of gout, the monosodium urate crystal, is described here. In suspensions of washed platelets, response to urate crystals proceeded in two phases: A secretory phase involved the rapid active release of serotonin, ATP, and ADP with little loss of lactic dehydrogenase or beta-glucuronidase. A lytic phase involved the slower loss of all platelet constituents. Both phases were inhibited by iodoacetate plus dinitrophenol, suggesting an energy requirement. In ultrastructural studies, lysis of washed platelets which appeared to contain crystals was seen. Urate crystals were also shown to induce serotonin release and platelet lysis in citrated platelet-rich plasma. Since urate crystals are deposited at a variety of sites, urate crystal-platelet interaction in vivo is a possibility. Such interactions, leading to release of platelet constituents, might contribute to gouty inflammation or to enhanced atherogenesis.
本文描述了痛风的病原体尿酸钠晶体导致人血小板成分的释放。在洗涤过的血小板悬液中,对尿酸盐晶体的反应分两个阶段进行:分泌阶段涉及5-羟色胺、三磷酸腺苷(ATP)和二磷酸腺苷(ADP)的快速主动释放,而乳酸脱氢酶或β-葡萄糖醛酸酶几乎没有损失。溶解阶段涉及所有血小板成分的较慢损失。两个阶段均受到碘乙酸盐加二硝基苯酚的抑制,提示需要能量。在超微结构研究中,可见似乎含有晶体的洗涤过的血小板发生溶解。尿酸盐晶体还显示可在枸橼酸化的富含血小板血浆中诱导5-羟色胺释放和血小板溶解。由于尿酸盐晶体沉积在多种部位,因此尿酸盐晶体与血小板在体内发生相互作用是有可能的。这种导致血小板成分释放的相互作用可能会导致痛风性炎症或增强动脉粥样硬化的发生。