Joukar Siyavash, Ghorbani-Shahrbabaki Soodabe
Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Science, Kerman, Iran.
Sleep Breath. 2016 May;20(2):787-93. doi: 10.1007/s11325-015-1299-3. Epub 2015 Dec 30.
Some of the previous studies have used animal model of paradoxical sleep deprivation for investigation of sleep loss complications. The present study is designed to examine the effectiveness and reliability of this model for investigation and assessment of some cardiovascular complications of obstructive sleep apnea syndrome.
The Wistar rat groups were divided into the control group, the Test48 and Test72 groups, who experienced paradoxical sleep deprivation for 48 and 72 h, and the Sham48 and Sham72 groups, who were exposed to environmental conditions same to test groups but without sleep deprivation, respectively. At the end of the experiment, blood pressure and heart rate variability were assessed.
The results showed that 72 h rapid eye movements sleep deprivation significantly increased the systolic blood pressure compared to the control (p < 0.01), Sham48 and Test48 groups (p < 0.05). The comparison of the heart rate and heart rate variability parameters such as time domain indices (RR interval, SDNN, RMSSD, SD1, SD2, and SD1/SD2) as well as frequency-domain variables (total power, LF and HF power, and LF/HF) had no significant difference among animal groups.
These findings suggest that rat paradoxical sleep deprivation may be a suitable model for induction and investigation of hemodynamic alterations which occurs in obstructive sleep apnea syndrome; however, it cannot be an alternative model to induce heart rate variability alterations similar to those reported in patient with obstructive sleep apnea.
先前的一些研究使用了异相睡眠剥夺动物模型来研究睡眠缺失并发症。本研究旨在检验该模型在调查和评估阻塞性睡眠呼吸暂停综合征的一些心血管并发症方面的有效性和可靠性。
将Wistar大鼠组分为对照组、经历48小时和72小时异相睡眠剥夺的Test48组和Test72组,以及分别暴露于与测试组相同环境条件但无睡眠剥夺的Sham48组和Sham72组。实验结束时,评估血压和心率变异性。
结果显示,与对照组(p < 0.01)、Sham48组和Test48组(p < 0.05)相比,72小时快速眼动睡眠剥夺显著升高了收缩压。动物组之间在心率和心率变异性参数(如时域指标(RR间期、SDNN、RMSSD、SD1、SD2和SD1/SD2)以及频域变量(总功率、LF和HF功率以及LF/HF))的比较上没有显著差异。
这些发现表明,大鼠异相睡眠剥夺可能是诱导和研究阻塞性睡眠呼吸暂停综合征中发生的血流动力学改变的合适模型;然而,它不能作为诱导类似于阻塞性睡眠呼吸暂停患者所报告的心率变异性改变的替代模型。