Vascular consequences of intermittent hypoxia.
Vascular consequences of intermittent hypoxia.
复制标题
间歇性缺氧的血管后果。
DOI：
10.1007/978-0-387-75434-5_6
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发表时间：
2007
影响因子：
--
通讯作者：
Morgan,BarbaraJ
中科院分区：
文献类型：
--
作者：
Morgan,BarbaraJ
在阻塞性睡眠呼吸暂停（OSA）患者中，夜间暴露于间歇性缺氧会导致动脉压升高，并持续一整天。动物模型表明，这种高血压效应需要完整的交感神经系统和完整的颈动脉化学感受器反射。在该模型中，肾素-血管紧张素系统对高血压起重要作用，因为肾神经去神经支配、血管紧张素II受体阻断和高盐饮食对肾素-血管紧张素系统的抑制都阻止了血压的升高。在该模型中以及OSA患者中，血管内皮功能受损。这些个体表现出血浆一氧化氮代谢物水平降低，中性粒细胞产生超氧化物增加，呼吸冷凝液中8-异前列烷水平升高。还存在促炎细胞因子水平升高。因此，氧化应激和炎症是间歇性缺氧诱导的血管功能障碍的潜在介质。一旦了解了间歇性缺氧引起的血管结构和功能改变的机制，就可以制定逆转或预防它们的策略。这些研究不仅与高血压有关，而且与动脉粥样硬化和OSA的其他重要心血管后遗症有关。
In patients with obstructive sleep apnea (OSA), nocturnal exposure to intermittent hypoxia causes elevations in arterial pressure that persist throughout the day. Animal models have shown that this hypertensive effect requires an intact sympathetic nervous system and an intact carotid chemoreceptor reflex. The reninangiotensin system contributes importantly to hypertension in this model, because renal nerve denervation, angiotensin II receptor blockade, and suppression of the renin-angiotensin system by high salt diet all prevent the rise in blood pressure. The vascular endothelium is functionally impaired in this model and also in patients with OSA. These individuals demonstrate decreased plasma levels of nitric oxide metabolites, increased production of superoxide by neutrophils, and increased levels of 8-isoprostane in breath condensate. Increased levels of pro-in- flammatory cytokines are also present. Thus, oxidant stress and inflammation are potential mediators of intermittent hypoxia-induced vascular dysfunction. Once the mechanisms of intermittent hypoxia-induced alterations in vascular structure and function are understood, strategies can be developed to reverse or prevent them. Such research has relevance not only to hypertension, but also to atherosclerosis and other important cardiovascular sequelae of OSA.