Department of Physiology, Faculty of Medicine, Trakya University; Edirne-Turkey.
Department of Physiotherapy and Rehabilitation, Trakya University; Edirne-Turkey.
Anatol J Cardiol. 2021 Jun;25(6):407-413. doi: 10.14744/AnatolJCardiol.2020.42205.
Recent community-based studies have identified sleep deprivation (SD) as an important modifiable risk factor for hypertension However, the underlying mechanisms linking SD to hypertension remain elusive. Thus, this study investigates blood pressure (BP) responses to cardiac autonomic stress tests in the presence of SD. Furthermore, we analyzed vascular inflammatory biomarkers as a possible underlying factor linking SD to increased BP.
Ten healthy male volunteers (age, 21.6±1.2 years) underwent repeated autonomic stress tests for three consecutive days (baseline, SD, and recovery). The autonomic stress tests included the Valsalva maneuver, mental arithmetic, isometric handgrip, and cold pressor tests. Each day, resting BPs were measured, venous blood samples were collected for intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin measurements, and stress tests were performed between 0900 and 1100. Ambulatory BP was recorded during the entire SD period (24 h).
One-night SD abolished BP reactivity to the Valsalva maneuver, isometric hand grip, and cold pressor tests, which returned after recovery sleep. Ambulatory BP monitoring showed that the mean systolic and diastolic BPs were 121.1±8.5 mm Hg and 72.8±6.3 mm Hg, respectively, between 0700 and 2300 and 120.3±9.6 mm Hg and 74.1±6.1 mm Hg, respectively, between 2300 and 0700 during the SD day (p>0.05 for both). Vascular inflammatory markers seemed unrelated to BP changes.
Acute SD altered BP responses to cardiac autonomic stress tests in healthy men without affecting resting BP levels. SD led to a non-dipping pattern in BP oscillation. Collectively, these findings highlight the importance of sleep in regulating BP.
最近的基于社区的研究已经确定睡眠剥夺(SD)是高血压的一个重要可改变的危险因素。然而,将 SD 与高血压联系起来的潜在机制仍不清楚。因此,本研究调查了 SD 状态下心脏自主应激试验对血压(BP)的反应。此外,我们分析了血管炎症生物标志物作为将 SD 与血压升高联系起来的一个可能的潜在因素。
10 名健康男性志愿者(年龄 21.6±1.2 岁)连续 3 天进行重复自主应激试验(基线、SD 和恢复)。自主应激试验包括瓦尔萨尔瓦动作、心算、等长握力和冷加压试验。每天测量静息血压,采集静脉血样测量细胞间黏附分子 1、血管细胞黏附分子 1 和 E-选择素,应激试验在 0900 至 1100 之间进行。在整个 SD 期间(24 小时)记录动态血压。
一夜 SD 消除了对瓦尔萨尔瓦动作、等长握力和冷加压试验的 BP 反应性,这些反应在恢复性睡眠后恢复。动态血压监测显示,SD 日 0700 至 2300 之间的平均收缩压和舒张压分别为 121.1±8.5mmHg 和 72.8±6.3mmHg,2300 至 0700 之间分别为 120.3±9.6mmHg 和 74.1±6.1mmHg(两者均 p>0.05)。血管炎症标志物似乎与 BP 变化无关。
急性 SD 改变了健康男性对心脏自主应激试验的 BP 反应,而不影响静息 BP 水平。SD 导致 BP 波动呈非杓型。总之,这些发现强调了睡眠在调节 BP 中的重要性。