Divisions of Pediatric Pulmonary, Allergy, and Critical Care Medicine, Stanford University Medical School Medicine, 770 Welch Road, Suite 350, Stanford, CA, 94305, USA.
Adv Exp Med Biol. 2010;661:201-20. doi: 10.1007/978-1-60761-500-2_13.
The increase in oxygen tension occurring at birth causes sustained and progressive pulmonary vasodilation. The oxygen-induced perinatal pulmonary vasodilation depends on the production of nitric oxide (NO) from the pulmonary endothelium and activation of various K(+) channels in pulmonary artery smooth muscle cells. This chapter reviews a) the oxygen-sensing mechanism that stimulates endothelial NO production; b) how K(+) channels sense changes in oxygen tension; c) whether hypoxia-inducible factor-1alpha (HIF-1alpha), a well defined hypoxia-sensitive transcription factor in adult, contributes to the regulation of NO production and K(+) channel activation; and d) whether and how dysfunctional K(+) channels contribute to the development of pulmonary hypertension in the newborns.
出生时氧张力的增加导致持续和渐进的肺血管舒张。氧诱导的围产期肺血管舒张依赖于肺内皮细胞产生的一氧化氮(NO)和肺动脉平滑肌细胞中各种 K(+)通道的激活。本章综述了:a)刺激内皮细胞产生 NO 的氧感应机制;b)K(+)通道如何感知氧张力的变化;c)在成人中作为明确的缺氧敏感转录因子的缺氧诱导因子-1α(HIF-1α)是否有助于 NO 产生和 K(+)通道激活的调节;d)K(+)通道功能障碍是否以及如何导致新生儿肺动脉高压的发展。