Effect of Thrombolysis on Circulating Microparticles in Patients with ST-Segment Elevation Myocardial Infarction.

IF 3.4 4区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Therapeutics Pub Date : 2023-11-18 eCollection Date: 2023-01-01 DOI:10.1155/2023/5559368

Zhe Li, Wei Zhang, Qun-Rang Wang, Yu-Juan Yang, Xin-Hong Liu, Gong Cheng, Feng-Jun Chang

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引用次数: 0

Abstract

Objective: We demonstrated that circulating microparticles (MPs) are increased in patients with coronary heart disease (both chronic coronary syndrome (CCS) and acute coronary syndrome). Whether thrombolysis affects MPs in patients with ST-segment elevation myocardial infarction (STEMI) with or without percutaneous coronary intervention (PCI) is unknown.

Methods: This study was divided into three groups: STEMI patients with thrombolysis (n = 18) were group T, patients with chronic coronary syndrome (n = 20) were group CCS, and healthy volunteers (n = 20) were the control group. Fasting venous blood was extracted from patients in the CCS and control groups, and venous blood was extracted from patients in the T group before (pre-T) and 2 hours after (post-T) thrombolysis. MPs from each group were obtained by centrifugation. After determining the concentration, the effects of MPs on endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in rat myocardial tissue in vitro were detected by immunohistochemistry and western blotting. Changes in nitric oxide (NO) and oxygen free radicals (O₂^•-) were also detected. The effect of MPs on vasodilation in isolated rat thoracic aortae was detected.

Results: Compared with that in the control group (2.60 ± 0.38 mg/ml), the concentration of MPs was increased in patients with CCS (3.49 ± 0.72 mg/ml) and in STEMI patients before thrombolysis (4.17 ± 0.58 mg/ml). However, thrombolysis did not further increase MP levels (post-T, 4.23 ± 1.01 mg/ml) compared with those in STEMI patients before thrombolysis. Compared with those in the control group, MPs in both CCS and STEMI patients before thrombolysis inhibited the expression of eNOS (both immunohistochemistry and western blot analysis of phosphorylation at Ser1177), NO production in the isolated myocardium and vasodilation in vitro and stimulated the expression of iNOS (immunohistochemistry and western blot analysis of phosphorylation at Thr495), and the generation of O₂^•- in the isolated myocardium. The effects of MPs were further enhanced by MPs from STEMI patients 2 hours after thrombolysis.

Conclusion: Changes in MP function after thrombolysis may be one of the mechanisms leading to ischemia-reperfusion after thrombolysis.

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溶栓对st段抬高型心肌梗死患者循环微粒的影响。

目的:我们证明冠心病(慢性冠状动脉综合征和急性冠状动脉综合征)患者的循环微粒(MPs)增加。溶栓是否影响st段抬高型心肌梗死(STEMI)伴或不伴经皮冠状动脉介入治疗(PCI)的MPs尚不清楚。方法:本研究分为三组:STEMI溶栓患者(n = 18)为T组，慢性冠状动脉综合征患者(n = 20)为CCS组，健康志愿者(n = 20)为对照组。取CCS组和对照组患者的空腹静脉血，取T组溶栓前(T前)和溶栓后2小时(T后)患者的静脉血。离心提取各组MPs。确定浓度后，采用免疫组化和免疫印迹法检测MPs对体外培养大鼠心肌组织内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)的影响。同时检测一氧化氮(NO)和氧自由基(O2•-)的变化。观察MPs对离体大鼠胸主动脉血管舒张的影响。结果:与对照组(2.60±0.38 mg/ml)相比，溶栓前CCS组MPs浓度升高(3.49±0.72 mg/ml)， STEMI组MPs浓度升高(4.17±0.58 mg/ml)。然而，与溶栓前的STEMI患者相比，溶栓并没有进一步提高MP水平(t后，4.23±1.01 mg/ml)。与对照组相比，溶栓前CCS和STEMI患者的MPs抑制了离体心肌中eNOS (Ser1177位点磷酸化的免疫组化和western blot分析)的表达、离体心肌中NO的产生和体外血管舒张，并刺激了离体心肌中iNOS (Thr495位点磷酸化的免疫组化和western blot分析)的表达和O2•-的产生。在溶栓2小时后，STEMI患者的MPs进一步增强MPs的作用。结论:溶栓后MP功能的改变可能是导致溶栓后缺血再灌注的机制之一。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cardiovascular Therapeutics 医学-心血管系统

CiteScore

5.60

自引率

0.00%

发文量

审稿时长

6 months

期刊介绍： Cardiovascular Therapeutics (formerly Cardiovascular Drug Reviews) is a peer-reviewed, Open Access journal that publishes original research and review articles focusing on cardiovascular and clinical pharmacology, as well as clinical trials of new cardiovascular therapies. Articles on translational research, pharmacogenomics and personalized medicine, device, gene and cell therapies, and pharmacoepidemiology are also encouraged. Subject areas include (but are by no means limited to): Acute coronary syndrome Arrhythmias Atherosclerosis Basic cardiac electrophysiology Cardiac catheterization Cardiac remodeling Coagulation and thrombosis Diabetic cardiovascular disease Heart failure (systolic HF, HFrEF, diastolic HF, HFpEF) Hyperlipidemia Hypertension Ischemic heart disease Vascular biology Ventricular assist devices Molecular cardio-biology Myocardial regeneration Lipoprotein metabolism Radial artery access Percutaneous coronary intervention Transcatheter aortic and mitral valve replacement.