Department of Physiology and Pathophysiology, Peking University, Health Science Center, Beijing, China.
Compr Physiol. 2011 Jan;1(1):61-79. doi: 10.1002/cphy.c090015.
Hypoxic pulmonary hypertension of the newborn is characterized by elevated pulmonary vascular resistance and pressure due to vascular remodeling and increased vessel tension secondary to chronic hypoxia during the fetal and newborn period. In comparison to the adult, the pulmonary vasculature of the fetus and the newborn undergoes tremendous developmental changes that increase susceptibility to a hypoxic insult. Substantial evidence indicates that chronic hypoxia alters the production and responsiveness of various vasoactive agents such as endothelium-derived nitric oxide, endothelin-1, prostanoids, platelet-activating factor, and reactive oxygen species, resulting in sustained vasoconstriction and vascular remodeling. These changes occur in most cell types within the vascular wall, particularly endothelial and smooth muscle cells. At the cellular level, suppressed nitric oxide-cGMP signaling and augmented RhoA-Rho kinase signaling appear to be critical to the development of hypoxic pulmonary hypertension of the newborn.
新生儿缺氧性肺动脉高压的特征是由于胎儿和新生儿期慢性缺氧导致血管重塑和血管张力增加，从而使肺血管阻力和压力升高。与成人相比，胎儿和新生儿的肺血管经历了巨大的发育变化，增加了对缺氧损伤的易感性。大量证据表明，慢性缺氧改变了各种血管活性物质的产生和反应性，如内皮衍生的一氧化氮、内皮素-1、前列腺素、血小板激活因子和活性氧，导致持续的血管收缩和血管重塑。这些变化发生在血管壁的大多数细胞类型中，特别是内皮细胞和平滑肌细胞。在细胞水平上，抑制性一氧化氮-cGMP 信号和增强的 RhoA-Rho 激酶信号似乎对新生儿缺氧性肺动脉高压的发展至关重要。
