血管氨酸转化酶活性的组织抑制可以在体内刺激血管生成
J E Fabre1, A Rivard, M Magner
1Departments of Medicine (Vascular Medicine) and Biomedical Research, St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, MA, USA.
Circulation
|June 15, 1999
概括
普利拉特抑制 ангиотензин转化酶 (ACE) 增强后肢缺血的子的血管生成. 这表明具有高组织亲和度的ACE抑制剂可能有助于在缺血病条件下治疗性血管生成.
科学领域:
- 血管生物学 血管生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 内皮细胞 (ECs) 对于产后血管生成至关重要.
- ангиотензин转化酶 (ACE) 抑制剂可以改善内皮功能.
研究的目的:
- 为了研究是否ACE抑制剂普利拉提升血管新生 in vivo.
- 为了比较奎纳普利特与卡波普利尔和血管内皮生长因子 (VEGF) 的作用.
主要方法:
- 使用后肢缺血的子模型.
- 子接受了奎纳普里拉,卡波普里尔,复合人体VEGF (rhVEGF) 或没有治疗.
- 血管生成通过血压,血管活性,抵抗,血管造影和毛细血管密度来评估.
主要成果:
- 奎那普里拉特显著增强了血管新生,与rhVEGF相当,优于卡波普里尔或对照剂.
- 奎那普利拉特有效地降低了组织的ACE活性,与卡普托普利尔不同.
- 功能和形态结局支持治疗麻治疗子的增强血管生成.
结论:
- 用普利抑制ACE可促进缺血后肢的血管生成.
- 具有高组织亲和度的非硫醇ACE抑制剂可能对治疗性血管生成有益.
- 在心肌缺血中ACE抑制的好处可能包括增强的附带发展.
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