Schulz R, Eisele H-J, Murzabekova G, Weissmann N
Medizinische Klinik II, Universitätsklinikum Giessen und Marburg, Standort Giessen.
Pneumologie. 2008 Jan;62(1):18-22. doi: 10.1055/s-2007-980132. Epub 2007 Oct 25.
Over the last decade the pathophysiology of obstructive sleep apnea (OSA)-related cardiovascular disease has been further elucidated in animal models employing dogs and rats/mice. It was demonstrated that, under the conditions of chronic intermittent hypoxia (CIH), endothelial dysfunction, i. e., a reduction in endothelial-dependent vasorelaxation, occurs. Furthermore, animals were shown to develop arterial hypertension when subjected to CIH for some weeks. Other aspects of the cardiovascular morbidity linked to OSA such as pulmonary hypertension, heart failure and atherosclerosis were also found in these animal models. The common result of these studies is that, apart from sympathetic over-activity, an increased oxidative stress seems to play a key role in the development of OSA-associated cardiovascular disease. It is anticipated that animal studies will continue to enhance our understanding of the pathogenesis of these disorders.
在过去十年中,阻塞性睡眠呼吸暂停(OSA)相关心血管疾病的病理生理学在使用犬类和大鼠/小鼠的动物模型中得到了进一步阐明。结果表明,在慢性间歇性缺氧(CIH)条件下,会出现内皮功能障碍,即内皮依赖性血管舒张功能降低。此外,动物在接受数周的CIH后会出现动脉高血压。在这些动物模型中还发现了与OSA相关的心血管疾病的其他方面,如肺动脉高压、心力衰竭和动脉粥样硬化。这些研究的共同结果是,除了交感神经过度活跃外,氧化应激增加似乎在OSA相关心血管疾病的发展中起关键作用。预计动物研究将继续增进我们对这些疾病发病机制的理解。