血小板聚集晨间增加的潜在机制：一项流式细胞术研究

Mechanisms underlying the morning increase in platelet aggregation: a flow cytometry study.

作者信息

Andrews N P, Gralnick H R, Merryman P, Vail M, Quyyumi A A

机构信息

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.

出版信息

J Am Coll Cardiol. 1996 Dec;28(7):1789-95. doi: 10.1016/S0735-1097(96)00398-1.

DOI:10.1016/S0735-1097(96)00398-1

PMID:8962568

Abstract

OBJECTIVES

Mechanisms underlying the morning increase in platelet aggregation produced by arising and assuming the upright posture were studied by examining 1) the expression on the platelet surface of activation-dependent markers; 2) platelet aggregation in whole blood; and 3) hematologic factors likely to influence aggregation.

BACKGROUND

The morning increase in thrombotic cardiovascular events has been attributed, in part, to the morning surge in platelet aggregability, but its mechanisms are poorly understood.

METHODS

Expression of seven platelet surface antigens (including P-selectin, activated GPIIb,IIIa and GPIb-IX), whole-blood platelet aggregation, platelet count and hematocrit were measured before and after arising in 17 normal volunteers. The fibrinolytic variables, tissue-type plasminogen activator, plasminogen activator inhibitor 1 and catecholamine levels were also measured.

RESULTS

On arising and standing, platelet aggregation increased by 71% (p < 0.01) and 27% (p < 0.03) in response to collagen and adenosine diphosphate, respectively. However, there was no change in any of the activation-dependent platelet surface markers. Whole-blood platelet count and hematocrit increased by 15% and 7% (both p < 0.0001), respectively. Norepinephrine and epinephrine levels increased by 189% (p < 0.0001) and 130% (p < 0.01), respectively. Tissue-type plasminogen activator antigen increased (31%, p < 0.01), but there was no significant increase in plasminogen activator inhibitor 1, suggesting an overall increase in fibrinolysis on standing. Prothrombin fragment 1.2 increased by 28% (p < 0.02), indicating a small increase in thrombin generation. The increases in hematocrit and platelet count that occurred on standing were carefully mimicked in vitro and resulted in a 115% (p < 0.05) increase in platelet aggregation in response to adenosine diphosphate.

CONCLUSIONS

These data demonstrate that the morning increase in platelet aggregation is not accompanied by expression of activation-dependent platelet surface receptors and suggest that the increase in whole-blood aggregation may be primarily due to the increases in catecholamine levels, platelet count and hemoconcentration.

摘要

目的

通过检测以下内容研究起床并采取直立姿势后血小板聚集在早晨增加的潜在机制：1）活化依赖性标志物在血小板表面的表达；2）全血中的血小板聚集；3）可能影响聚集的血液学因素。

背景

血栓性心血管事件在早晨的增加部分归因于早晨血小板聚集性的激增，但其机制尚不清楚。

方法

测量17名正常志愿者起床前后七种血小板表面抗原（包括P-选择素、活化的糖蛋白IIb/IIIa和糖蛋白Ib-IX）的表达、全血血小板聚集、血小板计数和血细胞比容。还测量了纤溶变量、组织型纤溶酶原激活物、纤溶酶原激活物抑制剂1和儿茶酚胺水平。

结果

起床并站立后，血小板对胶原和二磷酸腺苷的聚集分别增加了71%（p<0.01）和27%（p<0.03）。然而，任何活化依赖性血小板表面标志物均无变化。全血血小板计数和血细胞比容分别增加了15%和7%（均p<0.0001）。去甲肾上腺素和肾上腺素水平分别增加了189%（p<0.0001）和130%（p<0.01）。组织型纤溶酶原激活物抗原增加（31%，p<0.01），但纤溶酶原激活物抑制剂1无显著增加，提示站立时纤溶总体增加。凝血酶原片段1.2增加了28%（p<0.02），表明凝血酶生成略有增加。站立时发生的血细胞比容和血小板计数增加在体外被仔细模拟，并导致血小板对二磷酸腺苷的聚集增加了115%（p<0.05）。