Validation of pulse rate variability as a surrogate for heart rate variability in chronically instrumented rabbits

Pellegrino, Peter R.; Schiller, Alicia M.; Zucker, Irving H.

doi:10.1152/ajpheart.00898.2013

Cited by 17 publications

(14 citation statements)

References 29 publications

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“…This could be done by using blockade techniques for assessing the contribution of each branch of the ANS to PRV indices, or by comparing PRV results to more specific measurements such as microneurography. To the knowledge of the authors, the only blockade study that has been performed to evaluate changes in PRV was done by Pellegrino et al ( 2014 ). They showed that cardiovagal blockade induced an overestimation of HF measured from PRV; cardiac sympathetic blockade implied a moderate to high agreement between HRV and PRV in time- and frequency-domain indices; and dual blockade implied a poor accuracy and precision for normalized measures and LF/HF indices.…”

Section: Discussionmentioning

confidence: 99%

Heart Rate Variability (HRV) and Pulse Rate Variability (PRV) for the Assessment of Autonomic Responses

et al. 2020

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Introduction: Heart Rate Variability (HRV) and Pulse Rate Variability (PRV), are non-invasive techniques for monitoring changes in the cardiac cycle. Both techniques have been used for assessing the autonomic activity. Although highly correlated in healthy subjects, differences in HRV and PRV have been observed under various physiological conditions. The reasons for their disparities in assessing the degree of autonomic activity remains unknown. Methods: To investigate the differences between HRV and PRV, a whole-body cold exposure (CE) study was conducted on 20 healthy volunteers (11 male and 9 female, 30.3 ± 10.4 years old), where PRV indices were measured from red photoplethysmography signals acquired from central (ear canal, ear lobe) and peripheral sites (finger and toe), and HRV indices from the ECG signal. PRV and HRV indices were used to assess the effects of CE upon the autonomic control in peripheral and core vasculature, and on the relationship between HRV and PRV. The hypotheses underlying the experiment were that PRV from central vasculature is less affected by CE than PRV from the peripheries, and that PRV from peripheral and central vasculature differ with HRV to a different extent, especially during CE. Results: Most of the PRV time-domain and Poincaré plot indices increased during cold exposure. Frequency-domain parameters also showed differences except for relative-power frequency-domain parameters, which remained unchanged. HRV-derived parameters showed a similar behavior but were less affected than PRV. When PRV and HRV parameters were compared, time-domain, absolute-power frequency-domain, and non-linear indices showed differences among stages from most of the locations. Bland-Altman analysis showed that the relationship between HRV and PRV was affected by CE, and that it recovered faster in the core vasculature after CE. Conclusion: PRV responds to cold exposure differently to HRV, especially in peripheral sites such as the finger and the toe, and may have different information not available in HRV due to its non-localized nature. Hence, multi-site PRV shows promise for assessing the autonomic activity on different body locations and under different circumstances, which could allow for further understanding of the localized responses of the autonomic nervous system.

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Section: Discussionmentioning

confidence: 99%

Heart Rate Variability (HRV) and Pulse Rate Variability (PRV) for the Assessment of Autonomic Responses

et al. 2020

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“…After rabbits were put on telemetry jackets, their Lead II ECG signals in free and awake states were continuously monitored using EMKA non-invasive physiological signal telemetry system (EMKA, France) for 2 h. Then, HRV time-domain analysis was performed, and the indicators included the RR interval, SDNN, and RMSSD. In addition, frequency domain power spectrum analysis was performed according to the method previously studied [75], setting the VLF power as 0–0.0625 Hz, the LF power as 0.0625–0.1875 Hz and the HF power as 0.1875–2 Hz. Analysis indexes included TP, VLF, LF, and HF.…”

Section: Methodsmentioning

confidence: 99%

Royal Jelly Ameliorates Behavioral Deficits, Cholinergic System Deficiency, and Autonomic Nervous Dysfunction in Ovariectomized Cholesterol-Fed Rabbits

Pan

Jin

et al. 2019

Molecules

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Estrogen deficiency after menopause is associated with autonomic nervous changes, leading to memory impairment and increased susceptibility to Alzheimer’s disease (AD). Royal jelly (RJ) from honeybees (Apis mellifera) has estrogenic activity. Here, we investigated whether RJ can improve behavior, cholinergic and autonomic nervous function in ovariectomized (OVX) cholesterol-fed rabbits. OVX rabbits on high-cholesterol diet were administered with RJ for 12 weeks. The results showed that RJ could significantly improve the behavioral deficits of OVX cholesterol-fed rabbits and image structure of the brain. RJ reduced body weight, blood lipid, as well as the levels of amyloid-beta (Aβ), acetylcholinesterase (AchE), and malonaldehyde (MDA) in the brain. Moreover, RJ also increased the activities of choline acetyltransferase (ChAT) and superoxide dismutase (SOD) in the brain, and enhanced heart rate variability (HRV) and Baroreflex sensitivity (BRS) in OVX cholesterol-fed rabbits. Furthermore, RJ was also shown to reduce the content of Evans blue and the expression levels of Aβ, beta-site APP cleaving enzyme 1(BACE1), and receptor for advanced glycation end products (RAGE), and increase the expression level of LDL(low density lipoprotein) receptor-related protein 1 (LRP-1) in the brain. Our findings suggested that RJ has beneficial effects in neurological disorders of postmenopausal women, which were associated with reducing cholesterol and Aβ deposition, enhancing the estrogen levels and the activities of cholinergic and antioxidant systems, and ameliorating the blood–brain barrier (BBB) permeability and restoring autonomic nervous system.

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“…Heart rate variability (HRV) measurements were analyzed by the HRV analysis module in LabChart ® extracted from the pulse wave after passing through a 45 Hz low-pass filter. Normal to normal intervals were triggered by the maximal derivative of the pulse wave as this best correlates the interval extrapolated from the pulse wave to intervals generated by electrocardiogram (Pellegrino et al, 2014). Standard deviation of normal to normal (SDNN), root mean squared of the successive differences (RMSSD), and the low frequency (LF) (0.2 – 0.6 Hz) to high frequency (HF) (1.0–3.0 Hz) ratio (Erdos et al, 2015b) (LF/HF) were calculated using LabChart ® software.…”

Section: Methodsmentioning

confidence: 99%

Central TrkB blockade attenuates ICV angiotensin II-hypertension and sympathetic nerve activity in male Sprague-Dawley rats

Becker

Wang

Zucker

2017

Autonomic Neuroscience

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Increased sympathetic nerve activity and the activation of the central renin-angiotensin system are commonly associated with cardiovascular disease states such as hypertension and heart failure, yet the precise mechanisms contributing to the long-term maintenance of this sympatho-excitation are incompletely understood. Due to the established physiological role of neurotrophins contributing towards neuroplasticity and neuronal excitability along with recent evidence linking the renin-angiotensin system and brain-derived neurotrophic factor (BDNF) along with its receptor (TrkB), it is likely the two systems interact to promote sympatho-excitation during cardiovascular disease. However, this interaction has not yet been fully demonstrated, in vivo. Thus, we hypothesized that central angiotensin II (Ang II) treatment will evoke a sympatho-excitatory state mediated through the actions of BDNF/TrkB. We infused Ang II (20 ng/min) into the right lateral ventricle of male Sprague-Dawley rats for twelve days with or without the TrkB receptor antagonist, ANA-12 (50 ng/h). We found that ICV infusion of Ang II increased mean arterial pressure (+40.4 mmHg), increased renal sympathetic nerve activity (+19.4% max activity), and induced baroreflex dysfunction relative to vehicle. Co-infusion of ANA-12 attenuated the increase in blood pressure (−20.6 mmHg) and prevented the increase in renal sympathetic nerve activity (−22.2% max) and baroreflex dysfunction relative to Ang II alone. Ang II increased thirst and decreased food consumption, and Ang II + ANA-12 augmented the thirst response while attenuating the decrease in food consumption. We conclude that TrkB signaling is a mediator of the long-term blood pressure and sympathetic nerve activity responses to central Ang II activity. These findings demonstrate the involvement of neurotrophins such as BDNF in promoting Ang II-induced autonomic dysfunction and further implicate TrkB signaling in modulating presympathetic autonomic neurons during cardiovascular disease.

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Validation of pulse rate variability as a surrogate for heart rate variability in chronically instrumented rabbits

Cited by 17 publications

References 29 publications

Heart Rate Variability (HRV) and Pulse Rate Variability (PRV) for the Assessment of Autonomic Responses

Heart Rate Variability (HRV) and Pulse Rate Variability (PRV) for the Assessment of Autonomic Responses

Royal Jelly Ameliorates Behavioral Deficits, Cholinergic System Deficiency, and Autonomic Nervous Dysfunction in Ovariectomized Cholesterol-Fed Rabbits

Central TrkB blockade attenuates ICV angiotensin II-hypertension and sympathetic nerve activity in male Sprague-Dawley rats

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