Department of Pediatrics and Comer Children's Hospital, Pritzker School of Medicine, The University of Chicago, IL 60637, USA.
Sleep Med. 2010 Aug;11(7):714-20. doi: 10.1016/j.sleep.2009.12.013.
The cardiovascular consequences of obstructive sleep apnea syndrome (OSAS) in children have started to emerge over the last decade. It is clear that the respiratory and sleep alterations that characterize this relatively prevalent condition induce substantial alterations in autonomic nervous system control, ultimately generating high sympathetic outflow and reactivity that reflect an imbalance between sympatho-excitatory and vagal inhibitory inputs. In addition to these important consequences, the constitutive elements of OSAS also elicit a rather extensive activation of systemic inflammatory pathways that in turn pose substantial risk to the integrity and functional homeostasis of the endothelial network. The complex interactions between the multiple injury-associated pathways recruited by OSAS are further compounded by the potential release of angiogenic factors and by the mobilization and homing of progenitor cells that have the potential to repair and restore the OSAS-disrupted vascular function. Improved characterization of the mechanisms involved in every one of these processes and identification of the determinants of susceptibility in pediatric populations along with the interactions with obesity will clearly modify our approaches to OSAS in the future.
过去十年中，人们逐渐认识到阻塞性睡眠呼吸暂停综合征（OSAS）对儿童心血管系统的影响。很明显，这种相对普遍的疾病所具有的呼吸和睡眠改变会引起自主神经系统控制的实质性改变，最终导致交感神经传出和反应性增加，反映出交感兴奋和迷走抑制输入之间的不平衡。除了这些重要的后果外，OSAS 的构成要素还会引发全身性炎症途径的广泛激活，反过来又对内皮网络的完整性和功能动态平衡构成实质性威胁。OSAS 募集的多种损伤相关途径之间的复杂相互作用，加之血管生成因子的潜在释放以及祖细胞的动员和归巢，这些祖细胞有可能修复和恢复 OSAS 破坏的血管功能，使情况变得更为复杂。对这些过程中涉及的机制的更好描述，以及对儿科人群中易感性决定因素的识别，以及与肥胖的相互作用，将在未来明显改变我们对 OSAS 的处理方式。
