Sinisa M. Trbovic

Sleep apnea in normal and REM sleep-deprived normotensive Wistar-Kyoto and spontaneously hypertensive (SHR) rats

The effects of hypertension and REM sleep deprivation on spontaneous and postsigh apneas have been studied in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats by simultaneously monitoring their respiration and sleep by the EEG. The amount of REM and non-REM sleep in SHR rats was identical to WKY rats under control as well as REM sleep-deprived recording conditions. Hypertension was associated with an increase in postsigh apneas, as was evident by the increased postsigh apnea index in non-REM and total sleep in SHR rats when compared to normotensive WKY rats. In contrast, REM sleep deprivation suppressed the postsigh apnea expression both in non-REM and total sleep in SHR rats. The incidence of spontaneous apneas was increased by a combination of hypertension and REM sleep deprivation, as was shown in REM-deprived SHR rats, while each of these conditions alone had no effect on spontaneous apneas. These results suggest a role for hypertension in the postsigh apnea genesis and the existence of partially distinct mechanisms for the two types of apneas.

Effect of REM sleep deprivation on sleep apneas in rats

We studied the effects of 48 h of REM sleep deprivation on spontaneous and post-sigh central apneas in Sprague-Dawley rates by simultaneously monitoring sleep by the EEG and respiration for 6 h. During the recovery sleep following REM deprivation a decrease in post-sigh apneas occurred in total sleep. There was no change in spontaneous apneas. The results suggest the existence of partially distinct mechanisms for the two types of apneas.

Cardiopulmonary interactions following REM sleep deprivation in Sprague-Dawley rats

We characterized the effects of 48 h of rapid-eye-movement (REM) sleep deprivation on cardiovascular and respiratory variables and on sleep-related cardiopulmonary interactions in adult male Sprague-Dawley rats. Rats were instrumented for monitoring EEG, EMG, and aortic blood pressure. Respiratory rate and minute ventilation were measured by unrestrained single-chamber plethysmography. By using radiotelemetry to monitor blood pressure we clearly demonstrated progressive decreases in mean blood pressure with transitions from wakefulness to non-rapid-eye-movement and REM sleep which were unaffected by REM sleep deprivation. Mirror-image state-dependent increases in heart period suggest that baroreflexes were augmented during sleep with respect to wakefulness. REM sleep deprivation was also associated with lower blood pressure and longer heart period over all sleep/wake states, although this achieved statistical significance only during REM sleep and only during the first hour of recovery sleep. These cardiovascular changes coupled with the observed decreases in respiratory rate and minute ventilation suggest a further augmentation of baroreflexes following REM sleep deprivation.