失补偿性心力衰竭患者内皮细胞激活
Paolo C Colombo1, Javier E Banchs, Sulejman Celaj
1Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Circulation
|December 22, 2004
概括
在慢性心力衰竭 (CHF) 中,脱补偿激活静脉内皮,增加氧化应激标志物. 恢复到补偿状态显著减少了这种激活,并改善了血管功能.
科学领域:
- 心血管医学 心血管医学
- 血管生物学 血管生物学
- 心脏衰竭研究研究
背景情况:
- 在慢性心力衰竭 (CHF) 中,除了氧化 (NO) 之外的血管内皮功能尚不清楚.
- 慢性心血管疾病患者的动脉和静脉面临着类似的促炎媒介.
- 这项研究调查了失补偿性CHF中的静脉内皮细胞激活及其在补偿后的解决.
研究的目的:
- 为了确定静脉内皮是否在不补偿性慢性心血管疾病期间被激活.
- 为了评估这种激活是否会在患者恢复到补偿状态时消失.
- 为了将内皮细胞变化与血管功能标志物相关联.
主要方法:
- 研究了15名缺乏补偿的CHF患者和6名健康对照.
- 收集了静脉内皮细胞和血液;测量了手臂动脉流媒扩张 (FMD).
- 在无otropic 治疗前后评估了氨酸,循环氧化酶-2 (COX-2) 和诱导性 NO 合成酶 (iNOS) 的表达.
主要成果:
- 失补偿的CHF患者在静脉内皮和对照中的静脉内皮中显示出更高的尼托铁素,COX-2和iNOS.
- 补偿降低了尼托铁素,COX-2和iNOS的水平.
- 流媒扩张 (FMD) 得到改善,而血氧化应激标志物 (8-异波,双环芽素E2) 降低.
结论:
- 脱补偿性CHF与静脉内皮细胞激活有关.
- 导致补偿的短期内诺特洛普疗法显著降低了静脉内皮铁素,COX-2和iNOS的表达.
- 恢复补偿状态可以改善血管内皮功能.
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