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07:36
Angiogenesis in the Ischemic Rat Lung
Published on: February 8, 2013
缺血诱导的冠状动脉附带生长取决于血管内皮生长因子和氧化
T Matsunaga1, D C Warltier, D W Weihrauch
1Departments of Physiology and Anesthesiology, The Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, USA.
Circulation
|January 11, 2000
概括
氧化 (NO) 对于刺激冠状动脉附带生长至关重要,这是由缺血和血管内皮生长因子 (VEGF) 诱导的. 由VEGF诱导的抵押需要NO的生产.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 缺血症研究 缺血症研究
背景情况:
- 缺血症可以触发血管内皮生长因子 (VEGF) 的表达.
- 氧化 (NO) 的产生与刺激冠状动脉附带生长有关.
- 需要进一步调查VEGF,NO和抵押之间的相互作用.
研究的目的:
- 为了研究NO在缺血引起的冠状动脉附带生长中的作用.
- 确定VEGF表达和NO生产是否对刺激附带生长至关重要.
- 为了阐明VEGF诱导和NO信号在心肌缺血反应中的关系.
主要方法:
- 使用了一种重复性心肌缺血的狗模型.
- 用微球测量冠状动脉附带血流量.
- 通过西方分析和RT-PCR,在心肌间歇液中量化了VEGF表达.
- 氧化合成酶通过使用N(G) -nitro-L-arginine甲基 (L-NAME) 进行了对抗.
主要成果:
- 在对照犬中,重复性缺血逐渐增加了附带血流.
- NO合成酶与L-NAME的对抗性取消了附带血流的增加.
- 在对照组中,VEGF表达在早期达到峰值,但在L-NAME治疗的狗中,在整个缺血期间仍然升高.
- 反应性高血压,表明缺血的严重程度,随着对照中的附带担保增加而减少,但在NO被阻止时仍然强大.
结论:
- 氧化 (NO) 是冠状动脉附带生长的关键调节剂.
- 缺血诱导VEGF的表达,这是附带发展的关键因素.
- 由VEGF诱导的冠状动脉担保的过程取决于同时生产的NO.
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