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马尔凡综合征中的内皮功能:选择性损害流媒体血管扩张
D G Wilson1, M F Bellamy, M W Ramsey
1Congenital Heart Disease Center, University Hospital of Wales Healthcare NHS Trust, Heath Park, Cardiff, Wales, UK.
Circulation
|February 23, 1999
概括
马方综合征损害了流介导扩张,这是内皮细胞中纤维素的功能,但保留了激动剂介导扩张. 这表明纤维素是内皮机械转导和氧化释放的关键.
科学领域:
- 心血管研究的心血管研究.
- 血管生物学 血管生物学
- 结合组织疾病 结合组织疾病
背景情况:
- 马方综合征涉及纤维素的改变,影响血管结合组织.
- 纤维素微纤维素与动脉内皮细胞结合在一起,这表明它在内皮功能中起着作用.
- 在Marfan受试者的内皮细胞产物升高表明内皮功能障碍.
研究的目的:
- 直接评估Marfan受试者的流动和激素介导的内皮依赖的臂动脉反应性.
- 研究纤维素在内皮细胞功能和氧化释放中的作用.
- 在马凡综合征中区分流媒体和激素介导的内皮反应.
主要方法:
- 用超声波壁追踪,多普勒超声波和光电脉冲扫描来测量手臂动脉直径,血流和血压.
- 在手部高血压期间和酸甘油后评估了血管反应性.
- 还进一步评估了依赖内皮的血管扩张,使用动脉内注射乙胆,布拉迪基宁和NG-单甲基-L-阿尔金因 (L-NMMA).
主要成果:
- 与对照人群相比,马尔芬试验对象的流量介导臂动脉反应显著受损 (P<0.0001).
- 尼甘油诱导的血管扩张在两组中都是相似的,这表明保持了光滑肌肉功能.
- 抗激素诱导的血管扩张到乙胆和布拉迪基宁,以及L-NMMA诱导的血管收缩,在两组之间没有显著差异.
结论:
- 马尔凡受试者表现出受流介导的内皮依赖血管扩张受损,但保留了激素介导血管扩张.
- 这些发现表明,基底氧化释放可能在马凡综合征中被保留.
- 流介导扩张的选择性丧失突显了纤维素在内皮细胞机械传导中的潜在作用.
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