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[心血管疾病患者循环膜微粒的凝血活性]

[Coagulation activity of circulating membrane microparticles in patients with cardiovascular diseases].

作者信息

Antonova O A, Golubeva N V, Yakushkin V V, Zyuryaev I T, Krivosheeva E N, Komarov A L, Martynyuk T V, Mazurov A V

机构信息

National Medical Research Center of Cardiology, Russian Ministry of Health, Moscow, Russia.

出版信息

Biomed Khim. 2022 Aug;68(4):288-296. doi: 10.18097/PBMC20226804288.

Abstract

Membrane microparticles (MP) are released by activated or damaged cells and are able to accelerate blood clotting (coagulation). MP possess coagulation activity since all of them contain on their surface phosphatidylserine (PS), a substrate for the assembly of coagulation complexes, and some of them tissue factor (TF), the primary initiator of coagulation cascade reactions. We compared the coagulation activity and amount of MP in the blood of healthy donors (n=34) and patients with myocardial infarction (MI) (n=32), advanced atherosclerosis (AA) (n=32) and idiopathic pulmonary arterial hypertension (IPAH) (n=19). Total MP fraction was obtained from blood plasma by sedimentation at 20000 g, 30 min. The coagulation activity of PM isolated from 100 μl of donor and patient plasma was determined using a modified recalcification test. MP were added to substrate plasma devoid of endogenous MF, plasma was recalcified, and clotting was recorded by changes in optical density (A450), determining lag phase (min) and maximum rate (Vmax, %A450/min). MP were counted by flow cytometry as PS+ particles (lactadgerin-FITC staining) smaller than 1 μm and their concentration was expressed as 105 MP/μl plasma. MP in all patient groups accelerated plasma clotting more effectively than donor MP. Lag phase compared with donors (11.8 [11.0-13.1] median and interquartile range) was shorter in patients with AA (8.8 [7.0-10.3], p.

摘要

膜微粒(MP)由活化或受损细胞释放,能够加速血液凝固(凝血)。MP具有凝血活性,因为它们所有表面都含有磷脂酰丝氨酸(PS),这是凝血复合物组装的底物,并且其中一些含有组织因子(TF),即凝血级联反应的主要启动因子。我们比较了健康供体(n = 34)、心肌梗死(MI)患者(n = 32)、晚期动脉粥样硬化(AA)患者(n = 32)和特发性肺动脉高压(IPAH)患者(n = 19)血液中MP的凝血活性和数量。通过在20000 g下沉淀30分钟从血浆中获得总MP组分。使用改良的复钙试验测定从100 μl供体和患者血浆中分离出的PM的凝血活性。将MP添加到不含内源性MF的底物血浆中,血浆复钙,通过光密度变化(A450)记录凝血情况,确定延迟期(分钟)和最大速率(Vmax,%A450/分钟)。通过流式细胞术将MP计数为小于1 μm的PS +颗粒(乳杆菌素 - FITC染色),其浓度表示为105 MP/μl血浆。所有患者组中的MP比供体MP更有效地加速血浆凝血。与供体相比(中位数和四分位间距为11.8 [11.0 - 13.1]),AA患者的延迟期较短(8.8 [7.0 - 10.3],p。 (原文此处似乎不完整)

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