Asymmetry in sympathetic and vagal activities during sleep-wake transitions.

STUDY OBJECTIVES: To explore the role of autonomic nervous system in initiation of sleep-wake transitions. DESIGN: Changes in cardiovascular variability during sleep-wake transitions of adult male Wistar-Kyoto rats on their normal daytime sleep were analyzed. INTERVENTIONS: A 6-h daytime sleep-wakefulness recording session was performed. MEASUREMENTS AND RESULTS: Electroencephalogram and electromyogram (EMG) signals were subjected to continuous power spectral analysis, from which mean power frequency of the electroencephalogram (MPF) and power of the EMG were quantified. Active waking (AW), quiet sleep (QS), and paradoxical sleep (PS) were defined every 8 s according to corresponding MPF and EMG power. Continuous power spectral analysis of R-R intervals was performed to quantify its high-frequency power (HF, 0.6-2.4 Hz), low-frequency power (0.06-0.6 Hz) to HF ratio (LF/HF). MPF exhibited two phases of change during AW-QS and QS-AW transitions: a slowly changing first phase followed by a rapidly changing second phase. HF increased linearly with the decrease of MPF during the first phase of AW-QS transition whereas LF/HF increased linearly with the increase of MPF during the first phase of QS-AW transition. However, the LF/HF was not correlated with the HF. The MPF and HF exhibited only a rapidly changing phase during QS-PS transition. The LF/HF declined transiently during the QS-PS transition, followed by a sustained increase in PS. CONCLUSIONS: The parasympathetic activity before falling asleep and the sympathetic activity before waking up change coincidentally with EEG frequency, and may respectively contain the messages of sleeping and waking drives.

Regression analysis between heart rate variability and baroreflex-related vagus nerve activity in rats.

INTRODUCTION: Many previous studies have suggested that the high-frequency (HF) power of the heart rate variability may represent cardiac vagal activity although direct evidence of a correlation between the HF and vagal neuronal activity is still lacking. In the present study, we performed a regression analysis of the HF and vagal neurograms. METHODS AND RESULTS: Experiments were carried out on adult male Sprague-Dawley rats anesthetized with a continuous infusion of pentobarbital sodium. The baroreflex-related vagus neuronal activities were obtained by nerve or single-fiber recordings. The transient baroreflex response was employed to alter vagus neuronal activities using a bolus injection of phenylephrine (PE). On-line power spectral analysis of the heart rate and a vagal neurogram was performed during the acute baroreflex response. During the test period, systemic arterial pressure immediately increased in response to the PE injection, after which the R-R interval (RR), HF (0.6-2.4 Hz), and vagus nerve and unit activities all dramatically increased. Both nerve and unit activities exhibited good correlations (r > or = 0.7 in all nerve recordings and r > or = 0.6 in 91% of single-fiber recordings) with the HF. There were insignificant differences between the right- and left-side baroreflex-related vagus nerve recordings. CONCLUSION: Our present study provides a direct linkage between the HF and vagus neuronal electrical activity in anesthetized rats.

Sleep-related vagotonic effect of zolpidem in rats.

RATIONALE: Zolpidem is a relatively new nonbenzodiazepine sedative-hypnotic. The effects of zolpidem on autonomic functions remain unclear. OBJECTIVES: The aim of this study was to evaluate the effects of zolpidem on sleep and related cardiac autonomic modulations as compared with triazolam in Wistar-Kyoto rats. METHODS: Continuous power spectral analyses of electroencephalogram (EEG), electromyogram, and heart rate variability were performed on freely moving rats during daytime sleep. The consciousness states were classified into active waking (AW), quiet sleep (QS), and paradoxical sleep (PS). Drugs were administered via gavage and data within 2 h were analyzed. RESULTS: All zolpidem (ZP3, 3 mg/kg; ZP30, 30 mg/kg) and triazolam (TZ0.075, 0.075 mg/kg; TZ0.75, 0.75 mg/kg) groups had longer accumulated QS time and averaged QS duration as compared with the vehicle control. The accumulated QS time and averaged QS duration of ZP3 were similar to those of TZ0.075. Significant suppressions of PS time were noted in all drug groups except ZP3. During QS, ZP3 and ZP30 exhibited significant increases of magnitude and percentage of EEG delta power, whereas TZ0.075 and TZ0.75 did not. Heart period and high-frequency power of heart rate variability increased significantly in ZP3 during all sleep-wake states. Both parameters, however, did not increase but even decreased in ZP30, TZ0.075, and TZ0.75. CONCLUSIONS: Zolpidem not only caused a longer and deeper sleep but also led to an elevated cardiac vagal activity at a specific dose in the rat.

Changes in sleep patterns in spontaneously hypertensive rats.

STUDY OBJECTIVES: To explore whether spontaneous hypertension is associated with a change in sleep pattern in rats. DESIGN: Adult male spontaneously hypertensive rats (SHR) were compared to normotensive Wistar-Kyoto rats (WKY) on their normal daytime sleep pattern. PARTICIPANTS: Ten WKY and 10 SHR. INTERVENTIONS: All rats had electrodes implanted for polygraphic recordings. Weeks later, a 5-hour daytime sleep-weakfulness recording session was analyzed. MEASUREMENTS AND RESULTS: Electroencephalogram and electromyogram signals were subjected to continuous power spectral analysis, from which mean power frequency of the electroencephalogram and power of the electromyogram were quantified. Active waking (AW), quiet sleep (QS), and paradoxical sleep (PS) were defined every 8 seconds from corresponding mean power frequency and electromyogram power readings. Analysis of heart-rate variability was derived from the electrocardiogram signals. Macrostructural analysis of sleep revealed that SHR were characterized by fewer QS and PS episodes and eventually shorter accumulated QS and PS times as compared to WKY. SHR also had more QS-to-AW transitions but fewer QS-to-PS transitions. Microstructural analysis revealed that SHR were associated with more-frequent interruptions during QS. Analysis of heart-rate variability indicated that SHR had similar R-R intervals and lower high-frequency (0.6-2.4 Hz) power but a higher ratio of low-frequency (0.06-0.6 Hz) power to high-frequency power during the daytime recording as compared to WKY. CONCLUSIONS: As compared to WKY, SHR may have less sleep time, poorer sleep quality, and a greater tendency to wake up from QS. Such changes in sleep may be concomitant with cardiac autonomic changes. Our methodology offers a convenient yet effective way to study the constitution, sequence, and interruption of sleep in the rat.

Sleep-related sympathovagal imbalance in SHR.

The role of the autonomic nervous system in spontaneous hypertension during each stage of the sleep-wake cycle remains unclear. The present study attempted to evaluate the differences in cardiac autonomic modulations among spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), and Sprague-Dawley rats (SD) across sleep-wake cycles. Continuous power spectral analysis of electroencephalogram, electromyogram, and heart rate variability was performed in unanesthetized free moving rats during daytime sleep. Frequency-domain analysis of the stationary R-R intervals (RR) was performed to quantify the high-frequency power (HF), low-frequency power (LF)-to-HF ratio (LF/HF), and normalized LF (LF%) of heart rate variability. WKY and SD had similar mean arterial pressure, which is significantly lower than that of SHR during active waking, quiet sleep, and paradoxical sleep. Compared with WKY and SD, SHR had lower HF but similar RR, LF/HF, and LF% during active waking. During quiet sleep, SHR developed higher LF/HF and LF% in addition to lower HF. SHR ultimately exhibited significantly lower RR accompanied with higher LF/HF and LF% and lower HF during paradoxical sleep compared with WKY. We concluded that significant cardiac sympathovagal imbalance with an increased sympathetic modulation occurred in SHR during sleep, although it was less evident during waking.

Relationship between electroencephalogram slow-wave magnitude and heart rate variability during sleep in rats.

To explore whether depth of sleep is related to changes in autonomic control in rats, continuous power-spectral analysis of electroencephalogram (EEG) and heart rate variability (HRV) was performed in unanesthetized rats during normal daytime sleep. Quiet sleep (QS) was associated with an increase in high-frequency power of HRV (0.6-2.4 Hz, HF) but a decrease in low-frequency power (0.06-0.6 Hz) to HF ratio (LF/HF) compared with awakening. During QS, LF/HF was significantly and negatively correlated with delta power of EEG (0.5-4.0 Hz), whereas mean R-R interval and HF were not. As in humans, cardiac sympathetic regulation in rats is negatively related to the depth of sleep during QS, although vagal regulation is not. Our methodology offers a parallel way of studying the interaction between cerebral cortical and autonomic functions in rats.

A low-noise flexible integrated system for recording and analysis of multiple electrical signals during sleep-wake states in rats.

A low-noise flexible system for the simultaneous recording and analysis of several electrical signals (EEG, ECG, EMG, and diaphragm EMG) from the same rat was constructed for studying changes in physiological functions during the sleep-wake cycle. The hardware in the system includes a multichannel amplifier, a video camera, a timer code generator, and a PC. A miniature buffer headstage with high-input impedance connected to a 6-channel amplifier was developed. All electrical activities devoid of 60 Hz interference could be consistently recorded by our low-cost amplifier with no shielding treatment. The analytical software was established in the LabVIEW environment and consisted of three major frames: temporal, spectral, and nonlinear analyses. These analytical tools demonstrated several distinct utilities. For example, the sleep-wake states could be successfully distinguished by combining temporal and spectral analyses. An obvious theta rhythm during rapid-eye-movement sleep (REMS) was recorded from parietal to occipital cortical areas but not from the frontal area. In addition, two types of sleep apnea with/without cardiac arrhythmias were observed under REMS condition. Moreover, the evoked potentials of the primary somatosensory cortex elicited by innocuous electrical pulses were modulated by vigilant states, especially under a slow-wave sleep state. These results show that our system delivers high-quality signals and is suitable for sleep investigations. The system can be easily expanded by combining other recording devices, like a plethysmograph. This compact system can also be easily modified and applied to other related physiological or pharmacological studies.