TY - JOUR
T1 - Estimation of the baroreflex total loop gain by the power spectral analysis of continuous arterial pressure recordings
AU - Mannoji, Hiroshi
AU - Saku, Keita
AU - Nishikawa, Takuya
AU - Tohyama, Takeshi
AU - Kamada, Kazuhiro
AU - Abe, Kiyokazu
AU - Sunagawa, Genya
AU - Kishi, Takuya
AU - Sunagawa, Kenji
AU - Tsutsui, Hiroyuki
N1 - Funding Information:
H. Mannoji, T. Nishikawa, T. Takeshi, K. Kamada, K. Abe, and G. Sunagawa have nothing to declare. K. Saku and T. Kishi work in a department endowed by Omron Healthcare. K. Sunagawa works in a department endowed by Omron Healthcare and Actelion Pharmaceuticals, Japan. H. Tsutsui received honoraria from Daiichi Sankyo, Otsuka Pharmaceutical, Takeda Pharmaceutical, Mitsubishi Tanabe Pharma, Boehringer Ingelheim Japan, Novartis Pharma, Bayer Yakuhin, Bristol-Myers Squibb, and Astellas Pharma and research funding from Actelion Pharmaceuticals Japan, Daiichi Sankyo, and Astellas Pharma.
Funding Information:
This work was supported by the Japan Agency for Medical Research and Development (Grants JP18he1102003, JP18hm0102041, and JP18he1902003), Actelion Academia Prize 2015, and Grant-in-Aid for Young Scientists (B) from the Japan Society for the Promotion of Science (18K15893).
Publisher Copyright:
© 2019 the American Physiological Society.
PY - 2019/4
Y1 - 2019/4
N2 - Baroreflex dysfunction contributes to the pathogenesis of cardiovascular diseases. The baroreflex comprises a negative feedback loop to stabilize arterial pressure (AP); its pressure-stabilizing capacity is defined as the gain (G) of the transfer function (H) of the baroreflex total loop. However, no method exists to evaluate G in a clinical setting. A feedback system with H attenuates pressure disturbance (PD) to PD/(1 + H). We hypothesized that the baroreflex attenuates the power spectrum density (PSD) of AP in the baroreflex functioning frequency range. We created graded baroreflex dysfunction in rats using a modified sinoaortic denervation (SAD) method [SAD; control (no SAD): n = 9; partial SAD (SAD in the right carotid sinus): n = 6, and total SAD (SAD in the bilateral carotid sinuses): n = 6] and evaluated the PSD of 12-h telemetric AP recordings in the light phase. Using the ratio of PSD at 0.01- 0.1 Hz (PSD slope), we normalized them with the PSD in rats with complete baroreflex failure and derived the baroreflex index (BRI), which directly reflects G. We compared BRI and G obtained from a baroreflex open-loop experiment (reference G). The PSD slope became steeper with progression of baroreflex dysfunction. BRI (control: 2.00 ± 0.31, partial SAD: 1.28 ± 0.30, and total SAD: 0.06 ± 0.10, P < 0.05) was linearly correlated with reference G (R2 = 0.91, P < 0.01). BRI accurately estimated G of the baroreflex and may serve as a novel tool for estimating the pressure-stabilizing capacity of the baroreflex in clinical settings. NEW & NOTEWORTHY This study proposed a novel method to estimate the gain of the baroreflex total loop, the so-called “baroreflex indexA. (BRI). BRI focuses on action potential variability in the frequency domain, considering baroreflex low-pass filter characteristics within 0.01- 0.1 Hz. We demonstrated that BRI was linearly correlated with the reference gain of baroreflex in rats. Thus, BRI may contribute greatly to the development of a clinical tool for estimating baroreflex pressure-stabilizing capacity.
AB - Baroreflex dysfunction contributes to the pathogenesis of cardiovascular diseases. The baroreflex comprises a negative feedback loop to stabilize arterial pressure (AP); its pressure-stabilizing capacity is defined as the gain (G) of the transfer function (H) of the baroreflex total loop. However, no method exists to evaluate G in a clinical setting. A feedback system with H attenuates pressure disturbance (PD) to PD/(1 + H). We hypothesized that the baroreflex attenuates the power spectrum density (PSD) of AP in the baroreflex functioning frequency range. We created graded baroreflex dysfunction in rats using a modified sinoaortic denervation (SAD) method [SAD; control (no SAD): n = 9; partial SAD (SAD in the right carotid sinus): n = 6, and total SAD (SAD in the bilateral carotid sinuses): n = 6] and evaluated the PSD of 12-h telemetric AP recordings in the light phase. Using the ratio of PSD at 0.01- 0.1 Hz (PSD slope), we normalized them with the PSD in rats with complete baroreflex failure and derived the baroreflex index (BRI), which directly reflects G. We compared BRI and G obtained from a baroreflex open-loop experiment (reference G). The PSD slope became steeper with progression of baroreflex dysfunction. BRI (control: 2.00 ± 0.31, partial SAD: 1.28 ± 0.30, and total SAD: 0.06 ± 0.10, P < 0.05) was linearly correlated with reference G (R2 = 0.91, P < 0.01). BRI accurately estimated G of the baroreflex and may serve as a novel tool for estimating the pressure-stabilizing capacity of the baroreflex in clinical settings. NEW & NOTEWORTHY This study proposed a novel method to estimate the gain of the baroreflex total loop, the so-called “baroreflex indexA. (BRI). BRI focuses on action potential variability in the frequency domain, considering baroreflex low-pass filter characteristics within 0.01- 0.1 Hz. We demonstrated that BRI was linearly correlated with the reference gain of baroreflex in rats. Thus, BRI may contribute greatly to the development of a clinical tool for estimating baroreflex pressure-stabilizing capacity.
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U2 - 10.1152/ajpheart.00681.2018
DO - 10.1152/ajpheart.00681.2018
M3 - Article
C2 - 30608176
AN - SCOPUS:85063711888
VL - 316
SP - H828-H839
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6135
IS - 4
ER -