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亚司匹林触发的,循环氧基因酶-2-依赖的脂素合成调节了血管律
Pierre-Yves von der Weid1, Morley D Hollenberg, Stefano Fiorucci
1Mucosal Inflammation Research Group, University of Calgary, Calgary, Alberta, Canada.
Circulation
|August 25, 2004
概括
阿司匹林触发的素A ((4) 影响血管度和血压. 抑制素合成会放大阿司匹林的压力效应,强调素在心血管调节中的作用.
科学领域:
- 心血管生理学心血管生理学
- 炎症生物学 炎症生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 阿司匹林会触发15-R-epilipoxin A(4) (ATL) 的产生,这种蛋白质具有抗炎和胃保护作用.
- ATL对血管度的影响及其在阿司匹林心血管影响中的作用在很大程度上仍未被探索.
研究的目的:
- 调查ATL对阿司匹林诱导的血管调变化的贡献.
- 检查氧化 (NO) 在阿司匹林和ATL血管作用中介作用.
主要方法:
- 在活体中服用阿司匹林后评估血压 (BP) 的变化.
- 利用选择性循环氧化酶-2和5-脂氧化酶抑制剂,素受体对抗剂 (Boc2) 和中性粒细胞免疫减弱来调节ATL合成.
- 在孤立的老鼠大动脉和中枢动脉段中,确认了氧素A的血管松作用,评估了内皮依赖性.
主要成果:
- 静脉输入的素A (((4) 引起了血压的暂时降低.
- 阿司匹林增加了血清ATL和BP;抑制ATL合成显著增加了阿司匹林诱导的BP增加.
- 在孤立的动脉中诱导内皮依赖的血管松.
结论:
- 亚司匹林触发的素合成调节血管度和全身血压.
- 脂毒素在炎症反应期间可能在调节区域血流方面发挥作用.
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