Enhanced sympathetic outflow and decreased baroreflex sensitivity are associated with intermittent hypoxia-induced systemic hypertension in conscious rats

2006 ◽  
Vol 100 (6) ◽  
pp. 1974-1982 ◽  
Author(s):  
C. J. Lai ◽  
C. C. H. Yang ◽  
Y. Y. Hsu ◽  
Y. N. Lin ◽  
T. B. J. Kuo

Long-term exposure to intermittent hypoxia (IH), such as that occurring in association with sleep apnea, may result in systemic hypertension; however, the time course changes in arterial pressure, autonomic functions, and baroreflex sensitivity are still unclear. We investigated the changes in cardiovascular neural regulations during the development of chronic IH-induced hypertension in rats. Sprague-Dawley rats were exposed to repetitive 1.25-min cycles (30 s of N2 + 45 s of 21% O2) of IH or room air (RA) for 6 h/day during light phase (10 AM-4 PM) for 30 days. Arterial pressure was measured daily using the telemetry system during RA breathing. The mean arterial pressure (MAP) and interpulse interval (PPI) signals were then used to assess the autonomic functions and spontaneous baroreflex sensitivity by auto- and cross-spectral analysis, respectively. Stable MAP, low-frequency power of MAP (BLF), and low-frequency power (LF)-to-high frequency power (HF) ratio of PPI (LF/HF) were significantly higher in IH-exposed rats, compared with those of RA-exposed rats. Elevation of the MAP, BLF, LF/HF, and minute ventilation started 5 days after IH exposure and lasted until the end of the 30-day observation period. Additionally, IH-exposed rats had significant lower slope of MAP-PPI linear regression (under a successively descending and ascending) and magnitude of MAP-PPI transfer function (at frequency ranges of 0.06–0.6 Hz or 0.6–2.4 Hz) after IH exposure for 17 days. However, RA-exposed rats did not exhibit these changes. The results of this study indicate that chronic IH-induced hypertension is associated with a facilitation of cardiovascular sympathetic outflow and inhibition of baroreflex sensitivity in conscious rats.

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jing Guang ◽  
Halen Baker ◽  
Orilia Ben-Yishay Nizri ◽  
Shimon Firman ◽  
Uri Werner-Reiss ◽  
...  

AbstractDeep brain stimulation (DBS) is currently a standard procedure for advanced Parkinson’s disease. Many centers employ awake physiological navigation and stimulation assessment to optimize DBS localization and outcome. To enable DBS under sedation, asleep DBS, we characterized the cortico-basal ganglia neuronal network of two nonhuman primates under propofol, ketamine, and interleaved propofol-ketamine (IPK) sedation. Further, we compared these sedation states in the healthy and Parkinsonian condition to those of healthy sleep. Ketamine increases high-frequency power and synchronization while propofol increases low-frequency power and synchronization in polysomnography and neuronal activity recordings. Thus, ketamine does not mask the low-frequency oscillations used for physiological navigation toward the basal ganglia DBS targets. The brain spectral state under ketamine and propofol mimicked rapid eye movement (REM) and Non-REM (NREM) sleep activity, respectively, and the IPK protocol resembles the NREM-REM sleep cycle. These promising results are a meaningful step toward asleep DBS with nondistorted physiological navigation.


Epilepsia ◽  
2021 ◽  
Author(s):  
Abhijeet Gummadavelli ◽  
Reese Martin ◽  
Derek Goshay ◽  
Lim‐Anna Sieu ◽  
Jingwen Xu ◽  
...  

1981 ◽  
Vol 25 (1) ◽  
pp. 133-143 ◽  
Author(s):  
T. H. Jensen ◽  
F. W. McClain ◽  
H. Grad

Heating of a doublet plasma by driving an axisymmetric mode at low frequency may be an attractive means for auxiliary heating. The attractiveness of the method stems from (1) the low technology required for low-frequency power sources, (2) the fact that the field-shaping coils required for doublets may also be used as the antennae for transmitting the power, (3) the possibility of transmitting the power through a resistive vacuum wall, (4) the insensitivity to the plasma temperature and density and (5) the relative simplicity of the physical model. The utility of the concept depends on the existence of a special axisymmetric eigenmode in the resistive M.HD approximation which is used. This mode has nodes through the elliptic axes of the doublet equilibrium and an antinode at the hyperbolic axis. It is remarkable that the dissipation per cycle of this mode remains large at low plasma resistivity. This paper describes a linear theory for such heating.


2000 ◽  
Vol 278 (4) ◽  
pp. H1269-H1273 ◽  
Author(s):  
Cheryl C. H. Yang ◽  
Te-Chang Chao ◽  
Terry B. J. Kuo ◽  
Chang-Sheng Yin ◽  
Hsing I. Chen

Previous work from our laboratory using heart rate variability (HRV) has demonstrated that women before menopause have a more dominant parasympathetic and less effective sympathetic regulations of heart rate compared with men. Because it is still not clear whether normal or preeclamptic pregnancy coincides with alternations in the autonomic functions, we evaluated the changes of HRV in 17 nonpregnant, 17 normotensive pregnant, and 11 preeclamptic women who were clinically diagnosed without history of diabetic neuropathy, cardiac arrhythmia, and other cardiovascular diseases. Frequency-domain analysis of short-term, stationary R-R intervals was performed to evaluate the total variance, low-frequency power (LF; 0.04–0.15 Hz), high-frequency power (HF; 0.15–0.40 Hz), ratio of LF to HF (LF/HF), and LF in normalized units (LF%). Natural logarithm transformation was applied to variance, LF, HF, and LF/HF for the adjustment of the skewness of distribution. We found that the normal pregnant group had a lower R-R value and HF but had a higher LF/HF and LF% compared with the nonpregnant group. The preeclamptic group had lower HF but higher LF/HF compared with either the normal pregnant or nonpregnant group. Our results suggest that normal pregnancy is associated with a facilitation of sympathetic regulation and an attenuation of parasympathetic influence of heart rate, and such alterations are enhanced in preeclamptic pregnancy.


2019 ◽  
Author(s):  
Andria Pelentritou ◽  
Levin Kuhlmann ◽  
John Cormack ◽  
Steven Mcguigan ◽  
Will Woods ◽  
...  

B. AbstractBackground.Despite their intriguing nature, investigations of the neurophysiology of N-methyl-D-aspartate (NMDA)-antagonists Xenon (Xe) and nitrous oxide (N2O) are limited and have revealed inconsistent frequency-dependent alterations, in spectral power and functional connectivity. Discrepancies are likely due to using low resolution electroencephalography restricted to sensor level changes, concomitant anesthetic agent administration and dosage. Our intention was to describe the effects of equivalent stepwise levels of Xe and N2O administration on oscillatory source power using a crossover design, to explore universal mechanisms of NMDA-based anesthesia.Methods.22 healthy males participated in a study of simultaneous magnetoencephalography and electroencephalography recordings. In separate sessions, equivalent subanesthetic doses of gaseous anesthetic agents N2O and Xe (0.25, 0.50, 0.75 equi MAC-awake) and 1.30 MAC-awake Xe (for Loss of Responsiveness) were administered. Source power in various frequency bands was computed and statistically assessed relative to a conscious baseline.Results.Delta (l-4Hz) and theta (4-8Hz) band power was significantly increased at the highest Xe concentration (42%, 1.30 MAC-awake) relative to baseline for both magnetoencephalography and electroencephalography source power (p<0.005). A reduction in frontal alpha (8-13 Hz) power was observed upon N2O administration, and shown to be stronger than equivalent Xe dosage reductions (p=0.005). Higher frequency activity increases were observed in magnetoencephalographic but not encephalographic signals for N2O alone with occipital low gamma (30-49Hz) and widespread high gamma (51-99Hz) rise in source power.Conclusions.Magnetoencephalography source imaging revealed unequivocal and widespread power changes in dissociative anesthesia, which were divergent to source electroencephalography. Loss of Responsiveness anesthesia at 42% Xe (1.30 MAC-awake) demonstrated, similar to inductive agents, low frequency power increases in frontal delta and global theta. N2O sedation yielded a rise in high frequency power in the gamma range which was primarily occipital for lower gamma bandwidth (3049 Hz) and substantially decreased alpha power, particularly in frontal regions.Clinical trial number and Registry URLNot applicable.Prior PresentationsPelentritou Andria, Kuhlmann Levin; Lee Heonsoo; Cormack John; Mcguigan Steven; Woods Will; Sleigh Jamie; Lee UnCheol; Muthukumaraswamy Suresh; Liley David. Searching For Universal Cortical Power Changes Linked To Anesthetic Induced Reductions In Consciousness. The Science of Consciousness April 4th2018. Tucson, Arizona, USA.Summary StatementNot applicable.


1998 ◽  
Vol 274 (4) ◽  
pp. H1194-H1201 ◽  
Author(s):  
J. Andrew Taylor ◽  
Todd D. Williams ◽  
Douglas R. Seals ◽  
Kevin P. Davy

Low-frequency arterial pressure oscillations (Mayer waves) have been proposed as an index of vascular sympathetic outflow. However, cross-sectional differences in these pressure oscillations may not reflect different levels of sympathetic nervous outflow in humans. Three groups of healthy subjects with characteristically different sympathetic nervous outflow were studied: young females ( n = 10, 18–28 yr), young males ( n = 11, 18–29 yr), and older males ( n = 13, 60–72 yr). Average R-R interval, arterial pressures, and systolic pressure variability at the Mayer wave frequency (0.05–0.15 Hz) did not differ among the three groups. Diastolic pressure Mayer wave variability was similar in young females vs. young males (39 ± 10 vs. 34 ± 5 mmHg2) and lower in older males vs. young males (14 ± 2 mmHg2; P < 0.05). In contrast, muscle sympathetic activity was lowest in young females (892 ± 249 total activity/min) and highest in older males (3,616 ± 528 total activity/min; both P < 0.05 vs. young males: 2,505 ± 285 total activity/min). Across the three groups, arterial pressure Mayer wave variability did not correlate with any index of sympathetic activity. Our results demonstrate that arterial pressure Mayer wave amplitude is not a surrogate measure of vascular sympathetic outflow.


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