Division of Pulmonary and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Adv Exp Med Biol. 2010;661:221-35. doi: 10.1007/978-1-60761-500-2_14.
Exposure to prolonged alveolar hypoxia, as occurs with many chronic lung diseases or residence at high altitude, results in the development of pulmonary hypertension, significantly worsening patient prognosis. While the structural and functional changes that occur in the pulmonary vasculature in response to chronic hypoxia have been well characterized, less is known regarding the cellular mechanisms underlying this process. The use of animals models of hypoxic pulmonary hypertension have provided important insights into the changes that occur in the pulmonary vascular smooth muscle cells and some of the mediators involved. In this chapter, the effect of chronic hypoxia on various pulmonary arterial smooth muscle cell ion channels and transporters, and the role of the transcription factor, hypoxia-inducible factor 1, in regulating these changes, will be discussed.
长期肺泡缺氧会导致许多慢性肺部疾病或居住在高海拔地区,从而导致肺动脉高压,显著恶化患者的预后。虽然慢性缺氧引起的肺血管结构和功能变化已经得到很好的描述,但对于这一过程背后的细胞机制知之甚少。使用缺氧性肺动脉高压动物模型为肺血管平滑肌细胞发生的变化以及涉及的一些介质提供了重要的见解。在本章中,将讨论慢性缺氧对各种肺动脉平滑肌细胞离子通道和转运体的影响,以及转录因子缺氧诱导因子 1在调节这些变化中的作用。