Department of Medical Laboratory Techniques, Vocational School of Health Services, Marmara University, Istanbul, Turkey.
Chest Diseases Clinics, Fatih Sultan Mehmet Research and Education Hospital, Istanbul, Turkey.
Clinics (Sao Paulo). 2014;69(4):247-52. doi: 10.6061/clinics/2014(04)05.
Obstructive sleep apnea syndrome is characterized by repetitive obstruction of the upper airways, and it is a risk factor for cardiovascular diseases. There have been several studies demonstrating low levels of nitric oxide in patients with obstructive sleep apnea syndrome compared with healthy controls. In this study, we hypothesized that reduced nitric oxide levels would result in high arginase activity. Arginase reacts with L-arginine and produces urea and L-ornithine, whereas L-arginine is a substrate for nitric oxide synthase, which produces nitric oxide.
The study group consisted of 51 obstructive sleep apnea syndrome patients (M/F: 43/8; mean age 49±10 years of age) and 15 healthy control subjects (M/F: 13/3; mean age 46±14 years of age). Obstructive sleep apnea syndrome patients were divided into two subgroups based on the presence or absence of cardiovascular disease. Nitric oxide levels and arginase activity were measured via an enzyme-linked immunosorbent assay of serum samples.
Serum nitric oxide levels in the control subjects were higher than in the obstructive sleep apnea patients with and without cardiovascular diseases (p<0.05). Arginase activity was significantly higher (p<0.01) in obstructive sleep apnea syndrome patients without cardiovascular diseases compared with the control group. Obstructive sleep apnea syndrome patients with cardiovascular diseases had higher arginase activity than the controls (p<0.001) and the obstructive sleep apnea syndrome patients without cardiovascular diseases (p<0.05).
Low nitric oxide levels are associated with high arginase activity. The mechanism of nitric oxide depletion in sleep apnea patients suggests that increased arginase activity might reduce the substrate availability of nitric oxide synthase and thus could reduce nitric oxide levels.
阻塞性睡眠呼吸暂停综合征的特征是上呼吸道反复阻塞,是心血管疾病的危险因素。有几项研究表明,与健康对照组相比,阻塞性睡眠呼吸暂停综合征患者的一氧化氮水平较低。在这项研究中,我们假设一氧化氮水平降低会导致精氨酸酶活性升高。精氨酸酶与 L-精氨酸反应,产生尿素和 L-鸟氨酸,而 L-精氨酸是一氧化氮合酶的底物,可产生一氧化氮。
研究组包括 51 例阻塞性睡眠呼吸暂停综合征患者(男/女:43/8;平均年龄 49±10 岁)和 15 名健康对照者(男/女:13/3;平均年龄 46±14 岁)。根据是否存在心血管疾病,将阻塞性睡眠呼吸暂停综合征患者分为两组。通过酶联免疫吸附试验检测血清样本中的一氧化氮水平和精氨酸酶活性。
对照组的血清一氧化氮水平高于有和无心血管疾病的阻塞性睡眠呼吸暂停患者(p<0.05)。无心血管疾病的阻塞性睡眠呼吸暂停综合征患者的精氨酸酶活性明显更高(p<0.01),高于对照组。有心血管疾病的阻塞性睡眠呼吸暂停综合征患者的精氨酸酶活性高于对照组(p<0.001)和无心血管疾病的阻塞性睡眠呼吸暂停综合征患者(p<0.05)。
低水平的一氧化氮与高水平的精氨酸酶活性相关。睡眠呼吸暂停患者一氧化氮耗竭的机制表明,精氨酸酶活性增加可能会减少一氧化氮合酶的底物可用性,从而降低一氧化氮水平。