基底和刺激释放内源性氧化在孤立的人类肺部的血液动力学效应
G Cremona1, T W Higenbottam, E A Bower
1Pulmonary Division, "Salvatore Maugeri" Foundation IRCCS, Medical Centre, Veruno, Italy.
Circulation
|September 24, 1999
概括
肺高血压肺部内皮氧化 (NO) 释放受损,但基底NO释放仍然具有功能. 这项研究调查了NO的NO.
科学领域:
- 心血管科学 心血管科学
- 肺部医学 肺部医学
- 血管生物学 血管生物学
背景情况:
- 肺高血压 (PH) 是一种严重的疾病,影响肺血管系统.
- 内皮氧化 (NO) 在调节肺血管度方面起着至关重要的作用.
- 功能障碍的NO通路与PH的病理生理学有关.
研究的目的:
- 为了比较严重肺高血压 (SPH) 和慢性阻塞性肺病 (COLD) 患者与正常压力对照组在扩张的肺部中对NO通路调节的血液动力学反应.
- 为了研究不同肺部条件下的基底和刺激性内皮氧化 (NO) 释放的功能状态.
主要方法:
- 使用来自SPH,COLD和对照组的隔离透气肺.
- 在抑制NO合成 (N(G) - 尼特罗-L-阿尔金因甲基) 和刺激NO释放 (乙胆,酸) 的过程中测量了血液动力学反应.
- 分析了肺动脉压力 (PAP) 的变化,以评估血管反应.
主要成果:
- 在所有组中,NO合成的抑制导致了基线PAP的类似增加,这表明基线NO释放得到保存.
- 与对照组相比,用乙胆刺激NO释放导致SPH和COLD肺部的PAP减少明显较小.
- 酸在所有肺群体中有效降低了PAP,证实了光滑肌肉对外源NO的反应能力.
结论:
- 刺激性内皮氧化 (NO) 释放在肺动脉中的肺动脉受损,肺高血压或低血压肺高血压.
- 基本NO释放似乎即使在严重的肺高血压中也保持不变.
- 这些发现表明,PH肺中的刺激NO通路存在特定缺陷.
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