Mechanisms of intermittent hypoxia induced hypertension.

Mechanisms of intermittent hypoxia induced hypertension.
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DOI:
10.1111/j.1582-4934.2009.00929.x
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发表时间:
2010-01
影响因子:
5.3
通讯作者:
Kanagy NL
Kanagy NL
中科院分区:
医学2区
文献类型:
--
作者:
Bosc LV;Resta T;Walker B;Kanagy NL

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将啮齿类动物暴露于短暂的缺氧中,模拟了在阻塞性睡眠呼吸暂停(OSA)患者中观察到的低氧血症以及心血管和代谢效应,OSA是一种影响5%至20%人口的疾病。除了白天嗜睡,OSA还与全身性和肺动脉高压、外周血管疾病、中风和心源性猝死的高发病率相关。研究睡眠呼吸暂停的动物模型的发展提供了令人信服的证据,反复暴露于间歇性缺氧(IH)具有显着的血管和血液动力学的影响,解释了许多心血管疾病的发病率和死亡率观察到的睡眠呼吸暂停患者。然而,IH如何引起这些变化的分子和细胞机制尚不清楚,正在调查中。本审查的重点是最近的调查结果,解决这些机制。它包括一个讨论的神经系统,循环和血管因子,炎症介质和转录因子的IH诱导的心血管疾病的贡献。它还强调了活性氧作为全身性和肺动脉高压的主要介质的重要性,该介质是响应于暴露于IH而发展的。
Exposing rodents to brief episodes of hypoxia mimics the hypoxemia and the cardiovascular and metabolic effects observed in patients with obstructive sleep apnoea (OSA), a condition that affects between 5% and 20% of the population. Apart from daytime sleepiness, OSA is associated with a high incidence of systemic and pulmonary hypertension, peripheral vascular disease, stroke and sudden cardiac death. The development of animal models to study sleep apnoea has provided convincing evidence that recurrent exposure to intermittent hypoxia (IH) has significant vascular and haemodynamic impact that explain much of the cardiovascular morbidity and mortality observed in patients with sleep apnoea. However, the molecular and cellular mechanisms of how IH causes these changes is unclear and under investigation. This review focuses on the most recent findings addressing these mechanisms. It includes a discussion of the contribution of the nervous system, circulating and vascular factors, inflammatory mediators and transcription factors to IH-induced cardiovascular disease. It also highlights the importance of reactive oxygen species as a primary mediator of the systemic and pulmonary hypertension that develops in response to exposure to IH.
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