在实验性高胆固醇血清症中增强内甲素介导的冠状动脉收缩和减弱的基本氧化活性
V Mathew1, C R Cannan, V M Miller
1Division of Cardiovascular Diseases and Internal Medicine, Mayo Foundation, Rochester, Minn 55905, USA.
Circulation
|October 10, 1997
概括
实验性高胆固醇血症改变了冠状动脉血管运动反应. 甲基-1导致血管收缩增加,而氧化合成酶抑制效应减少,表明冠状动脉血管反应能力受损.
科学领域:
- 心血管生理学心血管生理学
- 内皮细胞功能 内皮细胞功能
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 实验性高胆固醇血症与冠状动脉血管功能障碍有关.
- 这项研究调查了冠状动脉血管运动对内素和氧化通路的反应变化,用于高胆固醇血症.
研究的目的:
- 为了测试实验性高胆固醇血清症改变冠状动脉血管运动对内素和内源性氧化 (NO) 途径抑制的假设.
主要方法:
- 在10周胆固醇饮食之前和之后,将Endothelin-1 (ET-1) 和N(G) - 单甲基-L-氨酸 (L-NMMA) 输入猪的冠状动脉.
- 测量冠状动脉血流 (CBF),冠状动脉直径 (CAD) 和冠状动脉血管阻力 (CVR).
- 对构成性氧化合成酶 (NOS) 的ET受体密度和免疫组织化学染色的评估.
主要成果:
- 患有高胆固醇血症的猪显示CBF和CAD显著显著下降,并且在对ET-1的反应中增加了CVR.
- 在高胆固醇贫血猪中,L-NMMA对CBF,CAD和CVR的影响减弱.
- 在高胆固醇贫血猪的冠状动脉中观察到构成性NOS免疫活性下降.
结论:
- 实验性高胆固醇血症增强了冠状动脉血管收缩到内.
- 在高胆固醇血症中,对抑制内源NO活性有减弱的反应.
- 这些发现表明,在实验性高胆固醇血症中冠状动脉血管反应的改变.
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