Ohga E, Nagase T, Tomita T, Teramoto S, Matsuse T, Katayama H, Ouchi Y
Department of Geriatric Medicine, Faculty of Medicine, University of Tokyo, Tokyo 113, Japan.
J Appl Physiol (1985). 1999 Jul;87(1):10-4. doi: 10.1152/jappl.1999.87.1.10.
Obstructive sleep apnea syndrome (OSAS) may be one of the most important risk factors of cardiovascular disorders, although the exact mechanism remains to be elucidated. In the present study, we hypothesized that OSAS-induced hypoxic stress might be involved in the etiology of cardiovascular disorders by activating adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and L-selectin. To examine this hypothesis, we measured circulating ICAM-1, VCAM-1, and L-selectin levels before and after sleep in OSAS patients and age-matched controls. The circulating ICAM-1, VCAM-1, and L-selectin levels increased in the OSAS patients before sleep compared with the normal subjects (ICAM-1: 392.9 +/- 48.5 vs. 201.2 +/- 55.0 ng/ml, P < 0.05; VCAM-1: 811.0 +/- 87.8 vs. 574.2 +/- 42.7 ng/ml, P < 0.05; L-selectin: 1,386.6 +/- 77.9 vs. 1,038.8 +/- 78.6 ng/ml, P < 0.01, respectively). After sleep, significantly greater levels of ICAM-1 and L-selectin, but not VCAM-1, were observed in the OSAS group. These observations suggest that OSAS-induced hypoxia activates adhesion molecules, resulting in the important risk factor of cardiovascular disorders. Treatment of OSAS can be, therefore, a potential approach to prevention of cardiovascular events.
阻塞性睡眠呼吸暂停综合征（OSAS）可能是心血管疾病最重要的危险因素之一，尽管确切机制仍有待阐明。在本研究中，我们假设OSAS诱导的低氧应激可能通过激活包括细胞间黏附分子1（ICAM-1）、血管细胞黏附分子1（VCAM-1）和L-选择素在内的黏附分子参与心血管疾病的病因。为检验这一假设，我们测量了OSAS患者和年龄匹配对照组睡眠前后循环中ICAM-1、VCAM-1和L-选择素的水平。与正常受试者相比，OSAS患者睡眠前循环中ICAM-1、VCAM-1和L-选择素水平升高（ICAM-1：392.9±48.5 vs. 201.2±55.0 ng/ml，P<0.05；VCAM-1：811.0±87.8 vs. 574.2±42.7 ng/ml，P<0.05；L-选择素：1386.6±77.9 vs. 1038.8±78.6 ng/ml，P<0.01）。睡眠后，OSAS组中ICAM-1和L-选择素水平显著升高，但VCAM-1未升高。这些观察结果表明，OSAS诱导的缺氧激活了黏附分子，导致了心血管疾病的重要危险因素。因此，治疗OSAS可能是预防心血管事件的一种潜在方法。
