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微血栓和纤维蛋白原样蛋白 2 在急性心肌缺血/再灌注大鼠无复流现象中的意义。

The significance of microthrombosis and fgl2 in no-reflow phenomenon of rats with acute myocardial ischemia/reperfusion.

机构信息

Department of Cardiology, Union Hospital of Huazhong, University of Science and Technology, Wuhan, Hubei Province, China.

出版信息

Clin Appl Thromb Hemost. 2013 Jan-Feb;19(1):19-28. doi: 10.1177/1076029612437577. Epub 2012 Mar 2.

DOI:10.1177/1076029612437577
PMID:22387586
Abstract

No-reflow phenomenon due to cardiac microvascular dysfunction or disturbance aggravates clinic outcomes of a portion of patients with acute myocardial infarction undergoing percutaneous coronary intervention or thrombolytic therapy. Our working hypothesis was that cardiac microthrombosis would play an important role in the pathogenesis. We investigated that cardiac microthrombi were observed by Martius, Scarlet, Blue methocl (MSB) and Masson trichrome staining. Furthermore, we investigated the expression of fibrinogen-like protein 2 (fgl2) in rats with acute myocardial ischemia/reperfusion (MI/R) and its possible pathological and clinical significance. The fgl2 was highly expressed in myocardium of rats with acute MI/R and located at cardiac microvascular walls. We found that the expression of fgl2 in peripheral mononuclear cells of rats with acute MI/R significantly increased correspondingly with its cardiac expression. Expression of cardiac fgl2 was correlated with no-reflow size of rats with acute MI/R, which was detected and calculated by thioflavin S staining. No-reflow size was in line with cardiac diastolic dysfunction of rats with acute MI/R monitored by hemodynamics. Thus, microthrombosis is involved in cardiac microvascular dysfunction or disturbance of rats with acute MI/R as one cause, and fgl2 may emerge as a predictor of the occurrence of no-reflow phenomenon.

摘要

无复流现象是由于心脏微血管功能障碍或紊乱引起的,它会加重部分接受经皮冠状动脉介入治疗或溶栓治疗的急性心肌梗死患者的临床预后。我们的工作假设是心脏微血栓在发病机制中起重要作用。我们通过 Martius、Scarlet、Blue methocl (MSB) 和 Masson 三色染色观察到心脏微血栓。此外,我们还研究了纤维蛋白原样蛋白 2 (fgl2) 在急性心肌缺血/再灌注 (MI/R) 大鼠中的表达及其可能的病理和临床意义。fgl2 在急性 MI/R 大鼠的心肌中高度表达,并位于心脏微血管壁上。我们发现,急性 MI/R 大鼠外周血单核细胞中 fgl2 的表达与心脏表达相应地显著增加。心脏 fgl2 的表达与急性 MI/R 大鼠的无复流面积相关,该面积通过硫代黄素 S 染色进行检测和计算。无复流面积与急性 MI/R 大鼠的心脏舒张功能障碍一致,这是通过血液动力学监测到的。因此,微血栓是急性 MI/R 大鼠心脏微血管功能障碍或紊乱的一个原因,fgl2 可能成为无复流现象发生的预测因子。

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