来自患有稳定胸痛患者的血小板中的酸盐耐药性
Y Y Chirkov1, A S Holmes, L P Chirkova
1Department of Cardiology, The Queen Elizabeth Hospital, University of Adelaide, Australia.
Circulation
|July 14, 1999
概括
稳定的胸痛患者的血小板对氧化物捐赠者如甘和酸的反应有所减少. 这种受损的血小板功能可能源于较低的冠酸环酶敏感性和增加的超氧化物水平.
科学领域:
- 心血管研究研究心血管研究
- 血小板生理学 血小板生理学
- 氧化信号传输 氧化信号传输
背景情况:
- 酸盐耐药性已知存在于心力衰竭中.
- 在患有稳定性胸痛 (SAP) 的患者中观察到类似的血小板对酸盐 (酸甘油和酸) 的反应减少的现象.
研究的目的:
- 在患有稳定性胸痛 (SAP) 的患者中研究血小板对氧化 (NO) 捐赠者的反应减弱.
- 探索导致这种现象的潜在机制,包括甘酸环酶敏感性和氧化应激,为这种现象做出贡献.
主要方法:
- 研究了NO捐赠体 (尼甘油和酸) 对二酸氨酸诱导的血小板聚合和血小板内循环单酸盐 (cGMP) 水平的影响.
- 利用ODQ,一种瓜尼酸环酶抑制剂,以及超氧化物脱酶/酶来评估NO信号和氧化应激的作用.
- 从正常受试者 (n=32) 和SAP患者 (n=56) 的血液样本中比较反应.
主要成果:
- 与正常受试者相比,Nitroglycerin和酸在SAP患者中显著减少了血小板聚合和cGMP升高的抑制.
- 来自SAP患者的血小板对NO捐赠者的敏感性降低,ODQ的抑制程度较低.
- 在SAP患者的血液中发现超氧化物 (O2-) 的含量增加,而超氧化物失调酶抑制了血小板聚合,并增强了SNP在这些患者中的抗聚合作用.
结论:
- SAP患者的血小板对NO捐赠者的抗聚合和cGMP刺激作用的反应较弱.
- 这种反应性降低可能是由于酸环酶对NO和NO因超氧化物无活化的敏感性降低.
- 缺陷的内源性NO (EDRF) 抗血小板活性可能会导致胸痛中血小板过度聚集.
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