西尔德纳菲尔抑制了缺氧诱导的肺高血压
L Zhao1, N A Mason, N W Morrell
1Section on Clinical Pharmacology, Imperial College School of Medicine, Hammersmith Hospital, London, UK.
Circulation
|July 27, 2001
概括
西尔德纳菲尔通过改善肺动脉压力,显著降低了人类和小鼠的缺氧诱导的肺高血压. 这种化酶5抑制剂提供了一种新的治疗方法,即使有损坏的氧化通路.
科学领域:
- 心血管生理学心血管生理学
- 药理学 药理学是指药理学的学科.
背景情况:
- 低氧会引发肺血管收缩,导致肺高血压.
- 像西尔代纳菲尔这样的基化酶5 (PDE5) 抑制剂正在针对心血管疾病进行研究.
研究的目的:
- 为了研究西尔代纳菲尔对人类和小鼠肺血管对缺氧反应的影响.
- 评估西尔代纳菲尔在减轻缺氧引起的肺高血压方面的疗效.
主要方法:
- 人类研究:随机,双盲试验,有10名志愿者在暴露于缺氧气体之前接受西尔代纳菲尔或安慰剂.
- 鼠标研究:与野生型和eNOS缺陷小鼠接触慢性缺氧的隔离透气肺和体内研究.
- 测量包括肺动脉压,全身血压,右心室缩压和心脏重塑标志物.
主要成果:
- 西尔德纳菲尔几乎消除了人类肺动脉压的缺氧增加,而不会影响全身血压.
- 在小鼠中,西尔代纳菲尔减轻了急性缺氧性肺血管收缩,并在慢性缺氧期间降低了右心室缩压和肺血管重塑.
- 药物的作用甚至在内皮氧化合成酶 (eNOS) 缺乏的小鼠中也被观察到,这表明了其他途径的贡献.
结论:
- 西尔德纳菲尔有效地减轻低氧诱导的肺高血压在人类和小鼠.
- 内皮氧化合成酶-氧化-循环瓜诺辛单酸盐 (eNOS-NO-cGMP) 途径参与其中,但其他cGMP来源也对西尔德纳菲尔的疗效有所贡献.
- 西尔德纳菲尔显示出有益的肺血液动力学效应,为肺高血压提供了潜在的治疗策略,即使eNOS活性受到损害.
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