张 倩, 张丙芳. 阻塞性睡眠呼吸暂停低通气综合征与高血压的相关分析[J]. 心脏杂志, 2015, 27(4): 486-489.
    引用本文: 张 倩, 张丙芳. 阻塞性睡眠呼吸暂停低通气综合征与高血压的相关分析[J]. 心脏杂志, 2015, 27(4): 486-489.
    Analysis of obstructive sleep apnea hypopnea syndrome and hypertension[J]. Chinese Heart Journal, 2015, 27(4): 486-489.
    Citation: Analysis of obstructive sleep apnea hypopnea syndrome and hypertension[J]. Chinese Heart Journal, 2015, 27(4): 486-489.

    阻塞性睡眠呼吸暂停低通气综合征与高血压的相关分析

    Analysis of obstructive sleep apnea hypopnea syndrome and hypertension

    • 摘要: 阻塞性睡眠呼吸暂停低通气综合征(OSAHS)是临床常见的慢性睡眠呼吸障碍性疾病。已有多项研究证实OSAHS与高血压密切相关,是高血压的独立危险因素之一。OSAHS引起持续高血压的原因尚不完全清楚,但多数学者认为,可能与OSAHS患者的睡眠结构紊乱致低氧血症、高碳酸血症刺激中枢和外周化学感受器导致交感神经系统兴奋,释放了较多的去甲肾上腺素,内皮素水平增高,内皮细胞依赖性血管释放因子减少,血管平滑肌严重肥厚并发生重构有关。OSAHS患者血压的大幅度波动,激活肾素-血管紧张素-醛固酮系统(RAAS)系统炎症因子增加,进一步导致了血管内皮功能紊乱。OSAHS常常引起持续性、难治性高血压,长期血压控制不佳更易并发靶器官损害。

       

      Abstract: Clinically, obstructive sleep apnea hypopnea syndrom (OSAHS) is a common chronic sleep breathing disorder. A number of studies have confirmed that OSAHS is closely related to hypertension and is one of the independent risk factors for hypertension. The cause of OSAHS-related persistent hypertension is not yet fully clear, but most scholars believe that disorder of sleep structure in OSAHS patients may cause hypoxemia and hypercapnia, which may stimulate the central and peripheral chemoreceptor, excite the sympathetic nervous system, release more norepinephrine, and subsequently increase endothelin levels. Then, dependent vascular endothelial cell release factors reduce, and serious vascular smooth muscle hypertrophy and remodeling occur. Significant blood pressure fluctuations in OSAHS patients may also activate RAAS system and increase inflammatory factors, further leading to vascular endothelial dysfunction. In addition, obesity and genetic factors may also play important roles in the development of OSAHS. OSAHS often causes persistent and refractory hypertension. Poor long-term control of blood pressure may lead to target organ damage.

       

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