Increased expression of endothelial-platelet dysfunctional pathway in patients with arterial erectile dysfunction.
Increased expression of endothelial-platelet dysfunctional pathway in patients with arterial erectile dysfunction.
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发表时间：
2011-10
影响因子：
1.4
通讯作者：
S. LaVignera
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作者：
S. LaVignera
目的属于血管壁（内皮损伤后）的特定物质的病理生理外化，通常不与血液（内膜下区域）接触，是表面受体血小板捕获的信号，导致其粘附。迄今为止，还没有研究检查动脉勃起功能障碍 (ED) 患者中这些受体的表达。本研究的目的是通过流式细胞术评估一系列选定的动脉 ED 患者且无明显其他缺血性动脉受累的患者中凋亡内皮微粒 (EMPa) 和玻连蛋白受体 (VR) 的血清浓度。方法连续评估 50 名选定的动脉 ED 患者（平均 IIEF-5 评分为 6.3±0.3，平均峰值收缩速度为 24.5±0.6 cm/s）。使用流式细胞仪进行EMPa和VR的评价。事件 CD45neg-CD144pos-annexinVpos 定义为 EMPa，而事件 CD51pos-CD61pos-CD41neg 定义为 VR。结果 动脉性ED患者的血清基线循环EMPa浓度（12.2±2.2% vs. 1.8±0.4%）和VR基线浓度（7.4±1.2% vs. 1.2±0.2%）显着高于对照组。结论 本研究表明，动脉 ED 患者内皮细胞凋亡和初始血小板粘附表达增加。
AIM Pathophysiological externalization of specific substances belonging to the vessel wall (after endothelial injury), usually not in contact with the blood (subintimal area) is the signal which is captured by surface receptor platelet's results in their adhesion. There are no studies that have so far examined the expression of these receptors in patients with arterial erectile dysfunction (ED). The aim of this study was to assess by flow cytometry, serum concentration of apoptotic endothelial microparticles (EMPa) and vitronectin receptor (VR) in a selected series of patients with arterial ED and without apparent other sistemic arterial involvement. METHODS Evaluated consecutively 50 selected patients with arterial ED-based (mean IIEF-5 score of 6.3±0.3 and mean peak systolic velocity of 24.5±0.6 cm/s). Evaluation of EMPa and VR was conducted using a flow cytometer. The events CD45neg-CD144pos-annexinVpos were defined EMPa, while events CD51pos-CD61pos-CD41neg were defined VR. RESULTS Patients with arterial ED had a serum baseline concentrations of circulating EMPa (12.2±2.2% vs. 1.8±0.4%) and VR (7.4±1.2% vs. 1.2±0.2%) significantly higher than control group. CONCLUSION The present study shows that patients with arterial ED had an increased expression of endothelial apoptosis and initial platelet adhesion.