在急性和慢性高homocysteinemia期间,内皮衍生型高极化因子介导的脏血管扩张反应受损
An S De Vriese1, Henk J Blom, Sandra G Heil
1Renal Unit, University Hospital, Gent, Belgium. an.devriese@azbrugge.be
Circulation
|May 1, 2004
概括
超homocysteinemia 损害了中的内皮衍生的高极化因子 (EDHF) 途径. 这种功能障碍影响小血管,可能导致微血管病变的发展.
科学领域:
- 血管生物学 血管生物学
- 脏生理学 脏生理学
- 内分泌学 在内分泌学.
背景情况:
- 内皮功能障碍是高血糖蛋白血症中血管问题的早期迹象.
- 内皮衍生的高极化因子 (EDHF) 对于调节小血管的血管度至关重要.
- 过高homocysteinemia对EDHF通路的影响以前是未知的.
研究的目的:
- 为了研究EDHF通路在脏微循环中的完整性.
- 评估急性和慢性高homocysteinemia对EDHF介导的血管扩张的影响.
主要方法:
- 通过脏血流对乙胆的反应评估EDHF介导的血管扩张.
- 系统抑制氧化合成酶和循环氧化原酶.
- 诱导性急性高homocysteinemia与homocysteine或氨酸; 慢性模型使用高氨酸饮食.
主要成果:
- 由于同类素的急性高homocysteinemia没有影响EDHF.
- 甲氨酸诱导的高血糖血症损害了EDHF介导的血管扩张.
- 慢性高homocysteinemia严重抑制EDHF介导的血管扩张,而内皮独立的血管扩张仍然完好无损.
结论:
- 在患有高homocysteinemia的老鼠的脏中,EDHF依赖的反应受损.
- 损坏EDHF功能对微血管病变的发展有重大影响.
- 这些发现突出了EDHF在与高血糖血症相关的血管并发症中的作用.
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