Pagani Massimo, Pizzinelli Paolo, Traon Anne Pavy-Le, Ferreri Cinzia, Beltrami Silvia, Bareille Marie-Pierre, Costes-Salon Marie-Claude, Béroud Stéphane, Blin Olivier, Lucini Daniela, Philip Pierre
Centro di Ricerca sulla Terapia Neurovegetativa, Dipartimento Scienze Cliniche L. Sacco, University of Milano, Milano, Italy.
Auton Neurosci. 2009 Jan 28;145(1-2):76-80. doi: 10.1016/j.autneu.2008.10.009. Epub 2008 Nov 8.
Sleep disorders are associated to a number of cardiovascular disturbances that might increase cardiovascular risk. Sleep deprivation, in particular, might, by inducing autonomic dysregulation, raise arterial pressure and hypertensive risk. Available evidence however is contradictory.
We tested the main hypothesis that one night sleep deprivation in 24 volunteers might alter hemodynamics (heart rate and Arterial Pressure - AP), autonomic regulation (mono and bivariate spectral analysis of RR and non invasive AP variability) and baroreflex control (spectral index alpha and spontaneous baroreflex slope), performance indices (reaction time) and subjective stress (questionnaires and salivary cortisol). Volunteers were studied in normal living conditions and while kept in isolation and confinement, to test the presence of possible bias related to environmental stress.
Results indicate that there were no differences between normal living conditions and isolation and confinement (Intraclass Correlation Coefficient >0.75 for most variables). Conversely, after one night sleep deprivation subjects felt tired (p<0.05), and performance deteriorated (p<0.05), while cortisol profile was substantially maintained, hemodynamic parameters did not change and HRV and index alpha increased slightly.
Findings support the contention that one night sleep deprivation, in absence of significant additional stress or disturbances, does not lead to increased arterial pressure values or to changes in autonomic or baroreflex profiles that could conceivably favor hypertension development, but induces the expected increase in tiredness and reduction in performance.
睡眠障碍与多种心血管紊乱有关，这些紊乱可能会增加心血管疾病风险。特别是睡眠剥夺，可能通过引起自主神经调节异常，升高动脉血压和高血压风险。然而，现有证据相互矛盾。
我们检验了主要假设，即24名志愿者一晚睡眠剥夺可能会改变血流动力学（心率和动脉血压 - AP）、自主神经调节（RR和无创AP变异性的单变量和双变量频谱分析）和压力反射控制（频谱指数α和自发性压力反射斜率）、性能指标（反应时间）以及主观应激（问卷调查和唾液皮质醇）。在正常生活条件下以及隔离和禁闭状态下对志愿者进行研究，以测试是否存在与环境应激相关的可能偏差。
结果表明，正常生活条件与隔离和禁闭状态之间没有差异（大多数变量的组内相关系数>0.75）。相反，一晚睡眠剥夺后，受试者感到疲倦（p<0.05），性能下降（p<0.05），而皮质醇水平基本保持不变，血流动力学参数未改变，HRV和指数α略有增加。
研究结果支持以下观点，即在没有明显额外应激或干扰的情况下，一晚睡眠剥夺不会导致动脉血压值升高，也不会导致自主神经或压力反射特征发生变化从而可能有利于高血压的发展，但会导致预期的疲劳增加和性能下降。
