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急性心肌梗死和稳定型心绞痛期间产生的微颗粒数量与血小板活化相关。

Number of microparticles generated during acute myocardial infarction and stable angina correlates with platelet activation.

机构信息

Department of Clinical Biochemistry, Jagiellonian University Medical College, Krakow, Poland.

出版信息

Arch Med Res. 2012 Jan;43(1):31-5. doi: 10.1016/j.arcmed.2012.01.006. Epub 2012 Feb 2.

Abstract

BACKGROUND AND AIMS

Elevated levels of circulating microparticles (MPs) have been reported in patients with acute myocardial infarction (AMI) and coronary artery disease. Platelet activation and inflammation have been recognized during AMI and stable angina (SA). We hypothesize that the origin and count of MPs in AMI and SA patients are related to markers of inflammation and platelet activation.

METHODS

Platelet, monocytes and endothelial MPs and surface P-selectin were determined in 12 AMI patients, 10 SA patients and 9 controls by flow cytometry. Plasma P-selectin, CD40 ligand (sCD40L) and interleukin 6 (IL-6) levels were evaluated by ELISA methods.

RESULTS

The total MP count was compared in control subjects, AMI, and SA patients: 12,765 (8465) vs. 38,750 (11,931) vs. 29,715 (12,072) counts/μl (p = 0.01), respectively. Patients with AMI displayed higher levels of total and platelet origin- tissue factor-positive (CD42/CD142) MPs than patients with SA: 72.8 (6.2) vs. 56.2 (6.4) %, p = 0.001. Levels of soluble P-selectin were significantly elevated in patients with AMI as compared to SA patients: 146 (6.5) vs. 107 (2.7) ng/mL, p = 0.005; significant correlation between total MP count and relative number of CD34, CD51, CD42-positive MPs, and the P-selectin expression was observed in patients with AMI.

CONCLUSIONS

Platelet activation in AMI is associated with increased generation of MPs not only from platelets, but also monocytes and endothelial cells. It suggests that interactions between platelets, monocytes and endothelial cells play an important role in the pathogenesis of myocardial ischemia.

摘要

背景和目的

已有研究报道,急性心肌梗死(AMI)和冠状动脉疾病患者的循环微颗粒(MPs)水平升高。在 AMI 和稳定性心绞痛(SA)期间已认识到血小板激活和炎症。我们假设 AMI 和 SA 患者 MPs 的起源和计数与炎症和血小板激活标志物有关。

方法

通过流式细胞术测定 12 例 AMI 患者、10 例 SA 患者和 9 例对照者的血小板、单核细胞和内皮 MPs 及表面 P-选择素。通过 ELISA 方法评估血浆 P-选择素、CD40 配体(sCD40L)和白细胞介素 6(IL-6)水平。

结果

在对照者、AMI 和 SA 患者中比较总 MP 计数:12765(8465)比 38750(11931)比 29715(12072)/μl(p = 0.01)。与 SA 患者相比,AMI 患者的总 MPs 和血小板起源组织因子阳性(CD42/CD142) MPs 水平更高:72.8(6.2)比 56.2(6.4)%,p = 0.001。与 SA 患者相比,AMI 患者可溶性 P-选择素水平显著升高:146(6.5)比 107(2.7)ng/mL,p = 0.005;在 AMI 患者中观察到总 MP 计数与 CD34、CD51、CD42 阳性 MPs 的相对数量以及 P-选择素表达之间存在显著相关性。

结论

AMI 中的血小板激活与 MPs 的产生增加有关,不仅来自血小板,而且来自单核细胞和内皮细胞。这表明血小板、单核细胞和内皮细胞之间的相互作用在心肌缺血的发病机制中起重要作用。

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