亲炎性调解剂通过一种依赖于氧化/循环GMP的机制,慢性地降低了动脉中由内皮衍生的高极化因子的形成
1Institut für Kardiovaskuläre Physiologie und Institut für Anaesthesiologie, Klinikum der J.W.G.-Universität, Frankfurt/Main, Germany.
Circulation
|April 13, 1999
概括
亲炎性调解剂通过诱导氧化合成酶II (NOSII) 在动脉中损害了内皮衍生的高极化因子 (EDHF) 的形成. 这种EDHF的减少有助于在动脉样硬化和败血症等疾病中导致内皮功能障碍.
科学领域:
- 血管生物学 血管生物学
- 内皮细胞功能 内皮细胞功能
- 炎症 炎症是一种炎症.
背景情况:
- 内皮依赖扩张器反应涉及氧化 (NO) 和EDHF.
- 这些反应在动脉样硬化和败血症中发生变化.
- 促炎媒介可能通过可诱导的NO合成酶 (NOS II) 影响EDHF生成.
研究的目的:
- 为了研究促炎媒介在孤立动脉中对EDHF产生的影响.
- 为了确定NOS II表达是否影响EDHF形成.
主要方法:
- 隔离的子动脉和猪冠状动脉暴露于细胞因子和脂多糖.
- 氧化合成酶 (NOS) 和环氧化原酶被阻断.
- 评估了NOS II表达和EDHF介导的放松.
- 测量了血管光滑肌肉细胞的高极化.
主要成果:
- 亲炎性调解剂显著减弱EDHF调解放松,与NOS II表达一致.
- 抑制NOS II或蛋白质合成可以防止这种松的放松.
- 没有捐赠者模仿了促炎媒介的效果.
- 亲炎性调解剂降低EDHF合成,降低了细胞染色体P450酶的表达.
结论:
- 亲炎性调解剂在隔离的动脉中抑制EDHF的形成.
- 这种抑制与NOS II表达有关,并且可能由诱导的NO生成介导.
- 减少EDHF形成可能导致动脉样硬化和败血症中的内皮功能障碍.
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