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在急性冠状动脉综合征中增加了血小板与循环单细胞的结合

Jaydeep Sarma¹, Caterina A Laan, Shirjel Alam

¹Medical Research Council Centre for Inflammation Research, University of Edinburgh Medical School, Edinburgh, UK. j.sarma@ed.ac.uk

|May 8, 2002

概括

在急性冠状动脉综合征中,血小板与单细胞的结合增加,在心肌梗塞患者中,一种新的独立于的通路升高. 这表明血管损伤的新治疗点.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
血液学血液学血液学

背景情况:

目前的急性冠状动脉综合征疗法侧重于血小板聚合.
血小板-白细胞相互作用与动脉壁疾病的进展有关.
在动物模型中,通过P-selectin glycoprotein ligand-1 (PSGL-1) 阻止血小板与白细胞的结合显示出有前途.

研究的目的:

为了研究血小板-单细胞相互作用在急性冠状动脉综合征中的作用.
为了确定参与血小板和单细胞结合的特定粘附机制.
探索心肌梗塞潜在的新型治疗点.

主要方法:

在外周血液样本中检查了血小板和单细胞的结合.
分析了健康捐赠者和患有急性冠状动脉综合征 (心痛不稳定,心肌梗塞) 和非心脏性胸痛的患者的粘附性.
评估了P-selectin依赖的和不依赖的结合成分.

主要成果:

在健康个体中,P-选择因-PSGL-1相互作用调解了大多数血小板-单细胞结合.
与对照人群相比,心肌梗塞和不稳定性胸痛患者的血小板和单细胞结合总量显著增加.
特别是在心肌梗塞患者中观察到独立于的血小板和单细胞结合的显著增加.

结论:

一个独立于P-选择因的机制有助于血小板-单细胞结合.
患有心肌梗塞和不稳定性胸痛的患者表现出高血小板-单细胞结合.
在心肌梗塞中增加的不依赖的粘附率表明了血管损伤的新型治疗点.

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