Objectives: A randomized controlled study of selective deprivation in different sleep periods of healthy volunteers was conducted to explore the effects of sleep deprivation on sleep structure,sleep-related respiratory events and inflammatory factors,and to explore the potential functional relationship between the three and the possible mechanism.To verify whether sleep deprivation is an independent risk factor for OSA,and to provide effective intervention targets for the whole life cycle management of patients with sleepdisordered breathing.Methods: According to the inclusion and exclusion criteria,30 healthy volunteers(male:female=1:1,mean age 26.27 ± 4.48years)were randomly divided into Rapid eye movement(REM)sleep deprivation group and Slow wave sleep(SWS)deprivation group.Both groups received polysomnography(PSG)for three consecutive nights,including baseline night,deprivation night and sleep recovery night.Under PSG monitoring,healthy volunteers were awakened for 5 minutes when the first polysomnography of REM sleep or SWS sleep appeared in both groups to ensure complete REM deprivation or SWS deprivation,The levels of TLR4,IRF3,My D88,IFN-α and TNF-α in serum were measured before and after deprivation.The data of sleep structure,nasal airflow and finger Oxygenation were analyzed.Results:(1)Compared with baseline night,REM sleep latency(L-REM)was shortened after REM deprivation(P<0.05),there was no significant difference in Total Sleep time(TST),Sleep efficiency(SE),Non-Rapid eye movement(NREM),Rapid eye movement(REM)Sleep and Rem%,SWS and SWS%,Wake after Sleep onset(WASO)(P>0.05);There was no significant difference in the recovery of sleep structure after SWS deprivation(P>0.05).(2)In comparison with the period before deprivation,the respiratory rate(RR)was significantly lower after REM deprivation(P<0.05),but there was no significant change in RR after SWS deprivation(P>0.05).the number of apnea(A),the number of hypopnea(H),the number of apnea-hypopnea(A + H),the apnea index(AI)and the apnea-hypopnea index(AHI)were significantly increased after SWS deprivation(P<0.05),there were no significant differences in hypopnea Index(HI),lowest Oxygenation Sa O2(LSa O2),mean Oxygenation Sa O2(MSa O2)and(P>0.05),but there were no significant differences in sleep breathing events after rem deprivation(P>0.05).(3)compared with pre-deprivation,the levels of TLR4,IRF3,My D88,IFN-α and TNF-αin SWS/REM group were significantly increased after deprivation(P<0.05).There was no significant difference in the expression of inflammatory factors between the two groups(P>0.05).(4)Correlation analysis of serum inflammatory factors and corresponding sleeprelated respiratory events found that,after REM deprivation,IRF3 concentration was negatively correlated with AI(r=-0.690,P=0.013)and AHI(r=-0.69,P=0.028).There was a negative correlation between the changes of My D88 and HI(r=-0.18,P=0.014).There was no significant correlation between the changes of TLR4,INF-α and TNF-α and the changes of sleep-breathing parameters(P>0.05).There was no significant correlation between the changes of inflammatory factors and sleep-related respiratory events after SWS deprivation(P>0.05).Conclusion:(1)Selective sleep deprivation had no significant effect on the structure of reentry sleep at night.(2)In this study,we found that sleep-related respiratory events such as A,H,A + H,AI,AHI increased after SWS sleep deprivation,but the breathing rate decreased after REM deprivation,and SWS sleep deprivation is a Independent risk factors for hypopnea events,sleep in the first half of the night has a greater impact on sleeprelated breathing events such as OSA(The first half of the night sleep is mainly SWS period).(3)The increased expression of TLR4,My D88,TNF-α,IRF3 and IFN-α after selective sleep deprivation may be related to the activation of TLR4 and other inflammatory pathways,short-term sleep therapy has the potential to suppress inflammation and reduce the body’s risk of inflammatory diseases.(4)The increase of AI and AHI after 1 night of REM deprivation may be related to the changes of IRF3,and the increase of HI may be related to the changes of Myd88. |