Siyavash Joukar1,2,3,4,5, Soodabe Ghorbani-Shahrbabaki6,7. 1. Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran. sjokar@gmail.com. 2. Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Science, Kerman, Iran. sjokar@gmail.com. 3. Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran. sjokar@gmail.com. 4. Department of Physiology and Pharmacology, Kerman University of Medical Sciences, Kerman, Iran. sjokar@gmail.com. 5. Siyavash Joukar, Neuroscience Research Center, Institute of Neuropharmacology, Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, and Department of Physiology and Pharmacology, School of Medicine, Kerman University of Medical Sciences, PO Box 7616914115, Kerman, Iran. sjokar@gmail.com. 6. Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Science, Kerman, Iran. 7. Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Abstract
PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
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