A method for assessment of the dynamic response of the arterial baroreflex

TY - JOUR

T1 - A method for assessment of the dynamic response of the arterial baroreflex

AU - Lund, Morten T

AU - Salomonsson, Max

AU - Jonassen, Thomas E N

AU - Holstein-Rathlou, Niels-Henrik

N1 - This article is protected by copyright. All rights reserved.

PY - 2018/2/1

Y1 - 2018/2/1

N2 - Aim: The baroreflex is a key mechanism in cardiovascular regulation, and alterations in baroreceptor function are seen in many diseases, including heart failure, obesity and hypertension. We propose a new method for analysing baroreceptor function from continuous blood pressure (BP) and heart rate (HR) in both health and disease. Methods: Forty-eight-hour data series of BP and HR were collected with telemetry. Sprague Dawley rats on standard chow (n = 11) served as controls, while rats on a high-fat, high-fructose (HFHC) diet (n = 6) constituted the obese-hypertensive model. A third group of rats underwent autonomic blockade (n = 6). An autoregressive–moving-average with exogenous inputs (ARMAX) model was applied to the data and compared with the α-coefficient. Results: Autonomic blockade caused a significant reduction in the strength of the baroreflex as estimated by ARMAX [ARMAX- baroreflex sensitivity (BRS)] −0.03 ± 0.01 vs. −0.19 ± 0.04 bpm heartbeat −1) . Both methods showed a ~50% reduction in BRS in the obese-hypertensive group compared with control (body weight 531 ± 27 vs. 458 ± 19 g, P < 0.05; mean arterial pressure 119 ± 3 vs. 102 ± 1 mmHg, P < 0.05; ARMAX-BRS −0.08 ± 0.01 vs. −0.15 ± 0.01 bpm heartbeat −1 , P < 0.05; α-coefficient BRS 0.51 ± 0.07 vs. 0.89 ± 0.07 ms mmHg −1 , P < 0.05). The ARMAX method additionally showed the open-loop gain of the baroreflex to be reduced by ~50% in the obese-hypertensive group (−2.3 ± 0.3 vs. −4.1 ± 0.3 bpm, P < 0.05), while the rate constant was similar between groups. Conclusion: The ARMAX model represents an efficient method for estimating several aspects of the baroreflex. The open-loop gain of the baroreflex was attenuated in obese-hypertensive rats compared with control, while the time response was similar. The algorithm can be applied to other species including humans.

AB - Aim: The baroreflex is a key mechanism in cardiovascular regulation, and alterations in baroreceptor function are seen in many diseases, including heart failure, obesity and hypertension. We propose a new method for analysing baroreceptor function from continuous blood pressure (BP) and heart rate (HR) in both health and disease. Methods: Forty-eight-hour data series of BP and HR were collected with telemetry. Sprague Dawley rats on standard chow (n = 11) served as controls, while rats on a high-fat, high-fructose (HFHC) diet (n = 6) constituted the obese-hypertensive model. A third group of rats underwent autonomic blockade (n = 6). An autoregressive–moving-average with exogenous inputs (ARMAX) model was applied to the data and compared with the α-coefficient. Results: Autonomic blockade caused a significant reduction in the strength of the baroreflex as estimated by ARMAX [ARMAX- baroreflex sensitivity (BRS)] −0.03 ± 0.01 vs. −0.19 ± 0.04 bpm heartbeat −1) . Both methods showed a ~50% reduction in BRS in the obese-hypertensive group compared with control (body weight 531 ± 27 vs. 458 ± 19 g, P < 0.05; mean arterial pressure 119 ± 3 vs. 102 ± 1 mmHg, P < 0.05; ARMAX-BRS −0.08 ± 0.01 vs. −0.15 ± 0.01 bpm heartbeat −1 , P < 0.05; α-coefficient BRS 0.51 ± 0.07 vs. 0.89 ± 0.07 ms mmHg −1 , P < 0.05). The ARMAX method additionally showed the open-loop gain of the baroreflex to be reduced by ~50% in the obese-hypertensive group (−2.3 ± 0.3 vs. −4.1 ± 0.3 bpm, P < 0.05), while the rate constant was similar between groups. Conclusion: The ARMAX model represents an efficient method for estimating several aspects of the baroreflex. The open-loop gain of the baroreflex was attenuated in obese-hypertensive rats compared with control, while the time response was similar. The algorithm can be applied to other species including humans.

KW - Journal Article

U2 - 10.1111/apha.12962

DO - 10.1111/apha.12962

M3 - Journal article

C2 - 28872781

SN - 1748-1708

VL - 222

JO - Acta Physiologica (Print)

JF - Acta Physiologica (Print)

IS - 2

M1 - e12962

ER -