高剂量的阿托瓦斯塔丁可以改善高胆固醇血清冠状动脉内皮功能障碍,而不会改善血管生成反应
Munir Boodhwani1, Yasunari Nakai, Pierre Voisine
1Division of Cardiothoracic Surgery and Cardiology, Beth Israel Deaconess Medical Center, 110 Francis St, LMOB 2A, Boston, Massachusetts 02215, USA.
Circulation
|July 6, 2006
概括
高剂量的阿托瓦斯塔丁在高胆固醇血清猪中改善了内皮功能,但没有增强心肌输液. 药物对血管生成的影响与分子变化有关,包括增加内静止素和降低血管内皮生长因子.
科学领域:
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
- 分子生物学分子生物学
背景情况:
- 3-基-3-甲基氨酸共酶A (HMG-CoA) 减少酶抑制剂 (他类药物) 已显示对心肌血管生成产生双相影响.
- 冠状动脉疾病中的内皮功能可以通过他类药物恢复.
- 研究高剂量阿托瓦斯塔丁对慢性心肌缺血症血管生成的影响至关重要.
研究的目的:
- 调查高剂量阿托瓦斯塔丁对内源性血管性反应的功能和分子影响.
- 评估阿托瓦斯塔丁对患有慢性缺血症的高胆固醇血症猪心肌血管生成的影响.
主要方法:
- 尤卡坦猪被养正常或高胆固醇饮食,有或没有阿托瓦斯塔丁 (每天3毫克/公斤) 13周.
- 慢性缺血是由阿梅洛伊德收缩器的放置引起的.
- 评估了微血管放松,心肌输液和蛋白质表达.
主要成果:
- 高胆固醇饮食损害了微血管放松,阿托瓦斯塔丁使其正常化.
- 在两个胆固醇养小组中,附带依赖心肌输液减少.
- 阿托瓦斯塔丁增加了Akt的酸化,降低了血管内皮生长因子,增加了内静止素的表达.
结论:
- 阿托瓦斯塔丁改善了高胆固醇血引起的内皮功能障碍,但没有改善附带依赖的输液.
- 增加的内静止素和降低的血管内皮生长因子表达,以及Akt激活,可能解释了血管新生反应的减少.
- 高剂量阿托瓦斯塔丁对血管生成的影响是复杂的,需要进一步研究.
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