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乙酰水杨酸对缺血性脑血管疾病患者血浆溶血磷脂酸水平的影响。

Influence of acetylsalicylate on plasma lysophosphatidic acid level in patients with ischemic cerebral vascular diseases.

作者信息

Li Zhen-Guang, Yu Zhan-Cai, Wang Dao-Zhen, Ju Wei-Ping, Zhan Xia, Wu Qi-Zhuan, Wu Xi-Juan, Cong Hai-Ming, Man Hong-Hao

机构信息

Department of Neurology, Wendeng Central Hospital, Weifang Medical College, Weifang, China.

出版信息

Neurol Res. 2008 May;30(4):366-9. doi: 10.1179/174313208X300369.

Abstract

BACKGROUND AND PURPOSE

Lysophosphatidic acid (LPA) is released from activated platelets. Acetylsalicylate (aspirin) is the most commonly used antiplatelet drug. The purpose of this study is to observe whether treatment with acetylsalicylate decreases the LPA level in patients with ischemic cerebrovascular diseases.

METHODS

We performed a study examining LPA level in fresh plasma in cases and controls enrolled in the LPA and Stroke Prevention Study. Level of LPA was assayed by measuring its inorganic phosphorus after separation by chromatography.

RESULTS

An elevated LPA level was seen in cases (n = 254) with ischemic cerebrovascular disease (3.11+/- 1.55 micromol/l) compared with 136 healthy controls (1.77 +/- 1.04 micromol/l) (p < 0.001). Administration of aspirin (100 mg q.d.) for 1 month significantly lowered LPA level in patients (n = 142) (2.41 +/- 1.03 mu mol/l) compared with that before taking acetylsalicylate (4.06 +/- 1.03 micromol/l) (p < 0.001). However, the LPA level in patients (n = 36) who stopped acetylsalicylate after taking it for 1 month was re-elevated. Before and after taking acetylsalicylate for 1 month, their LPA levels were 4.23 +/- 1.15 and 1.93 +/- 0.85 micromol/l, respectively. After 1 month withdrawal, level was 3.90 +/- 1.09 micromol/l (p < 0.001 compared that before taking acetylsalicylate).

CONCLUSION

Our findings support a close association between increased plasma LPA level and platelet activation. Acetylsalicylate could decrease plasma LPA levels, which may be used as a mechanism for acetylsalicylate in the prevention of ischemic stroke.

摘要

背景与目的

溶血磷脂酸(LPA)由活化血小板释放。乙酰水杨酸(阿司匹林)是最常用的抗血小板药物。本研究旨在观察乙酰水杨酸治疗是否能降低缺血性脑血管病患者的LPA水平。

方法

我们进行了一项研究,检测参与LPA与卒中预防研究的病例组和对照组新鲜血浆中的LPA水平。通过色谱分离后测量其无机磷来检测LPA水平。

结果

缺血性脑血管病病例组(n = 254)的LPA水平(3.11±1.55微摩尔/升)高于136名健康对照组(1.77±1.04微摩尔/升)(p < 0.001)。给予阿司匹林(100毫克/天)1个月后,患者组(n = 142)的LPA水平(2.41±1.03微摩尔/升)较服用乙酰水杨酸前(4.06±1.03微摩尔/升)显著降低(p < 0.001)。然而,服用乙酰水杨酸1个月后停药的患者组(n = 36)的LPA水平再次升高。服用乙酰水杨酸1个月前后,其LPA水平分别为4.23±1.15和1.93±0.85微摩尔/升。停药1个月后,LPA水平为3.90±1.09微摩尔/升(与服用乙酰水杨酸前相比,p < 0.001)。

结论

我们的研究结果支持血浆LPA水平升高与血小板活化密切相关。乙酰水杨酸可降低血浆LPA水平,这可能是乙酰水杨酸预防缺血性卒中的机制之一。

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