0086 SYSTOLIC BLOOD PRESSURE IS INCREASED DURING NON-REM SLEEP AFTER LIGHT-PHASE SLEEP FRAGMENTATION IN RATS

• Published in: Sleep (New York, N.Y.) N.Y.), 2017-04, Vol.40 (suppl_1), p.A33-A33
• Main Authors: Fink, AM, Mithani, S, Carley, DW
• Format: Article
• Language: English
• Subjects: Blood pressure; NREM sleep; REM sleep; Sleep
• ISSN: 0161-8105; 1550-9109
• DOI: 10.1093/sleepj/zsx050.085

Abstract Introduction: Occupational responsibilities (working night-shift, being on-call) can restrict and fragment sleep. We tested the hypothesis that sleep fragmentation (SF) has cardiovascular (CV) consequences by studying the impact of light-phase SF (LP-SF) on blood pressure (BP) and heart rate (HR) in Wistar-Kyoto (WKY) rats. Methods: WKY rats (N=5) were implanted with telemetry transmitters to measure electroencephalogram/electromyogram, electrocardiogram, and BP. Rats were acclimatized to light (LP; 0800-2000) and dark phases (DP; 2000-0800) and housed in SF chambers (Lafayette Neuroscience Co.). After obtaining baseline data (3 days), rats were recorded while mechanical arms continuously swept through the chambers (0800-1600) for 6 ± 2 consecutive days (each full sweep lasting 7.5 sec). Sleep was scored in 10 sec epochs. CV data were aggregated for wakefulness, rapid eye movement (REM) sleep, and non-REM sleep, which were compared across the LP-SF, LP-rest, and DP-rest periods (t-tests, repeated-measures ANOVA). Results: Compared with baseline sleep behaviors, the 8 hr LP-SF caused a 30% increase in non-REM sleep during the subsequent LP rest periods (1600–2000), but DP sleep-wake patterns were not significantly altered. Compared with LP baseline parameters between 1600–2000, the LP rest periods during this timeframe following SF were characterized by increased systolic BP during non-REM sleep (139 ± 4 mmHg [baseline], 147 ± 3 mmHg [last day], p=0.01) while associated HR responses did not differ significantly (363.3 ± 19 beats per min [bpm, baseline], 373 ± 26 bpm, p=0.5). None of the CV variables differed from baseline during REM sleep or during the DP. Collectively, these observations suggest that in nocturnal animals, LP-SF alters BP regulation in the subsequent rest period and that the impact on sleep and CV activities is reduced during the DP when rats are naturally more active. Conclusion: This experimental model allows for timed-periods of SF, an approach important for understanding the links among sleep, circadian rhythms, and CV disease risk. Future directions include measuring genetically-hypertensive WKY rats’ responses to both LP-SF and DP-SF to understand whether rats with existing hypertension also respond detrimentally to SF. Ultimately the work will guide the identification of CV disease risk reduction strategies for people with irregular work schedules. Support (If Any): Midwest Nursing Research Society.