Short-term regulation of arterial pressure and the calculation of open-loop gain in the intact anesthetized dog

1987 ◽  
Vol 15 (5) ◽  
pp. 427-441 ◽  
Author(s):  
R. Burattini ◽  
P. Borgdorff ◽  
N. Westerhof
Keyword(s):  
Arterial Pressure ◽  
Open Loop ◽  
Loop Gain ◽  
Short Term

Estimation of open-loop gain of canine arterial pressure control system by a new method

1981 ◽  
Vol 240 (6) ◽  
pp. H832-H836 ◽  
Author(s):  
H. Hosomi ◽  
K. Yokoyama
Keyword(s):  
Control System ◽  
Arterial Pressure ◽  
Pressure Change ◽  
Pressure Control ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Loop Gain ◽  
Reflex Gain ◽  
Pressure Control System ◽  
Arterial Pressure Control System

We developed a method to estimate an overall open-loop gain of the arterial pressure control system without surgically opening the reflex loop. Dogs anesthetized by intravenous injection of Nembutal (35 mg/kg body wt) were bled by 2 ml/kg body wt within 2-3 s through a catheter inserted into the abdominal aorta. Arterial pressure change after the quick hemorrhage was monitored via a catheter placed in the aortic arch for more than 2 min. The overall open-loop gain of the lumped arterial pressure control system was assessed as (delta API/delta APs)-1, where delta API is the immediate fall and delta APs the steady-state fall in mean arterial pressure obtained by a filter with a 2-s time constant. The advantage of this method is that the overall open-loop gain can be estimated under the closed-loop condition in which the baroreceptor reflexes operate naturally around the existing range of systemic arterial pressure. This enables one to study time-varying characteristics of the reflex gain. The disadvantage is that the substantial constituents of the lumped reflex system remain to be confirmed.

scholarly journals Diabetes mellitus attenuates the pressure response against hypotensive stress by impairing the sympathetic regulation of the baroreflex afferent arc

2019 ◽  
Vol 316 (1) ◽  
pp. H35-H44
Author(s):  
Kazuhiro Kamada ◽  
Keita Saku ◽  
Takeshi Tohyama ◽  
Toru Kawada ◽  
Hiroshi Mannoji ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Arterial Pressure ◽  
Control Theory ◽  
Open Loop ◽  
Pressure Response ◽  
Response Threshold ◽  
Loop Gain ◽  
Baroreflex Function ◽  
Sympathetic Regulation

Patients with diabetes mellitus (DM) often show arterial pressure (AP) lability associated with cardiovascular autonomic neuropathy. Because the arterial baroreflex tightly regulates AP via sympathetic nerve activity (SNA), we investigated the systematic baroreflex function, considering the control theory in DM by open-loop analysis. We used Zucker diabetic fatty (ZDF) rats as a type 2 DM model. Under general anesthesia, we isolated the carotid sinuses from the systemic circulation, changed intracarotid sinus pressure (CSP), and recorded SNA and AP responses. We compared CSP-AP (total loop), CSP-SNA (afferent arc), and SNA-AP (efferent arc) relationships between ZDF lean ( n = 8) and ZDF fatty rats ( n = 6). Although the total loop gain of baroreflex (ΔAP/ΔCSP) at the operating point did not differ between the two groups, the average gain in the lower CSP range was markedly reduced in ZDF fatty rats (0.03 ± 0.01 vs. 0.87 ± 0.10 mmHg/mmHg, P < 0.001). The afferent arc showed the same trend as the total loop, with a response threshold of 139.8 ± 1.0 mmHg in ZDF fatty rats. There were no significant differences in the gain of efferent arc between the two groups. Simulation experiments indicated a markedly higher AP fall and lower total loop gain of baroreflex in ZDF fatty rats than in ZDF lean rats against hypotensive stress because the efferent arc intersected with the afferent arc in the SNA unresponsive range. Thus, we concluded that impaired baroreflex sympathetic regulation in the lower AP range attenuates the pressure response against hypotensive stress and may partially contribute to AP lability in DM. NEW & NOTEWORTHY In this study, we investigated the open-loop baroreflex function, considering the control theory in type 2 diabetes mellitus model rats to address the systematic mechanism of arterial pressure (AP) lability in diabetes mellitus. The unresponsiveness of baroreflex sympathetic regulation in the lower AP range was observed in type 2 diabetic rats. It may attenuate the baroreflex pressure-stabilizing function and induce greater AP fall against hypotensive stress.

Baroreflex open-loop gain and arterial pressure compensation in hemorrhagic hypotension

1983 ◽  
Vol 245 (1) ◽  
pp. H54-H59 ◽  
Author(s):  
H. I. Chen ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Closed Loop ◽  
Control Level ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Loop Gain ◽  
Hemorrhagic Hypotension ◽  
Carotid Baroreceptor ◽  
Loop Condition ◽  
Pressure Compensation

The loop gain (G) of the carotid baroreceptor was determined using open- and closed-loop approach in anesthetized rabbits after aortic denervation and vagotomy. The open-loop relationship between the intrasinus pressure (ISP) and systemic arterial pressure (SAP) was nonlinear. The slope (delta SAP/delta ISP) or G was maximal (about 1.5) near the control arterial pressure and decreased toward the saturation pressures. We examined how this nonlinearity relates to the arterial pressure compensation following hemorrhage. Because the baroreflex attenuation of the posthemorrhagic hypotension depends on the SAP responses to an input perturbation, we first demonstrated that the open-loop responses in SAP to a specific delta ISP was not altered during various amounts of hemorrhage, despite different operating range for the responses. In the open-loop condition when ISP was fixed at the control level, hemorrhage of 10, 20, and 30 ml produced a SAP disturbance (D) of 23.3, 43.5, and 62.4 mmHg, respectively. The figures were minimized to 9.8, 19.8, and 34.4 mmHg (D'), respectively through the baroreflex compensation in the closed-loop condition. The calculated G (D/D' - 1) from the closed-loop data were 1.38, 1.20, and 0.82 for 10, 20, and 30 ml hemorrhage. For a given input signal (delta ISP = D'), the values of G were essentially the same as those obtained from the open-loop ISP-SAP curve. The G values decreased as the degree of hemorrhagic hypotension increased, being in agreement with the sigmoid characteristics of the nonlinear ISP-SAP curve.

scholarly journals Analytic and Integrative Framework for Understanding Human Sympathetic Arterial Baroreflex Function: Equilibrium Diagram of Arterial Pressure and Plasma Norepinephrine Level

2021 ◽  
Vol 15 ◽  
Author(s):  
Fumiyasu Yamasaki ◽  
Takayuki Sato ◽  
Kyoko Sato ◽  
André Diedrich
Keyword(s):  
Arterial Pressure ◽  
Equilibrium Diagram ◽  
Open Loop ◽  
Plasma Norepinephrine ◽  
Arterial Baroreflex ◽  
Loop Gain ◽  
Norepinephrine Level ◽  
Integrative Framework ◽  
Operating Points ◽  
Plasma Norepinephrine Level

BackgroundThe sympathetic arterial baroreflex is a closed-loop feedback system for stabilizing arterial pressure (AP). Identification of unique functions of the closed system in humans is a challenge. Here we propose an analytic and integrative framework for identifying a static operating point and open-loop gain to characterize sympathetic arterial baroreflex in humans.Methods and ResultsAn equilibrium diagram with two crossing functions of mechanoneural (MN) and neuromechanical (NM) arcs was analyzed during graded tilt maneuvers in seven healthy subjects. AP and plasma norepinephrine level (PNE), as a surrogate for sympathetic nerve activity, and were recorded after vagal modulation of heart function was blocked by atropine. The MN-arc curve was described as a locus of operating points during –7, 0, 15, and 60° head-up tilting (HUT) on a PNE-AP plane. The NM-arc curve was drawn as a line between operating points before and after ganglionic blockade (trimethaphan, 0.1 mg⋅ml–1⋅kg–1) during 0° or 15° HUT. Gain values were estimated from the slopes of these functional curves. Finally, an open-loop gain, which is a most important index for performance of arterial baroreflex, was given by a product of the gain values of MN (GMN) and NM arcs (GNM). Gain values of MN was 8.92 ± 3.07 pg⋅ml−1⋅mmHg−1; and GNM at 0° and 15° HUT were 0.61 ± 0.08 and 0.36 ± 0.05 mmHg⋅ml⋅pg–1, respectively. A postural change from supine to 15° HUT significantly reduced the open-loop gain from 5.62 ± 0.98 to 3.75 ± 0.62. The effects of HUT on the NM arc and open-loop gain seemed to be similar to those of blood loss observed in our previous animal studies.ConclusionAn equilibrium-diagram analysis contributes to a quantitative and integrative understanding of function of human sympathetic arterial baroreflex.

Counteraction of aortic baroreflex to carotid sinus baroreflex in a neck suction model

2000 ◽  
Vol 89 (5) ◽  
pp. 1979-1984 ◽  
Author(s):  
Toru Kawada ◽  
Masashi Inagaki ◽  
Hiroshi Takaki ◽  
Takayuki Sato ◽  
Toshiaki Shishido ◽  
...  
Keyword(s):  
Animal Model ◽  
Arterial Pressure ◽  
Linear Model ◽  
Closed Loop ◽  
Carotid Sinus ◽  
Open Loop ◽  
Pressure Perturbation ◽  
Loop Gain ◽  
First Approximation ◽  
Carotid Sinus Baroreflex

Although neck suction has been widely used in the evaluation of carotid sinus baroreflex function in humans, counteraction of the aortic baroreflex tends to complicate any interpretation of observed arterial pressure (AP) response. To determine whether a simple linear model can account for the AP response during neck suction, we developed an animal model of the neck suction procedure in which changes in carotid distension pressure during neck suction were directly imposed on the isolated carotid sinus. In six anesthetized rabbits, a 50-mmHg pressure perturbation on the carotid sinus decreased AP by −27.4 ± 4.8 mmHg when the aortic baroreflex was disabled. Enabling the aortic baroreflex significantly attenuated the AP response (−21.5 ± 3.8 mmHg, P< 0.01). The observed closed-loop gain during simulated neck suction was well predicted by the open-loop gains of the carotid sinus and aortic baroreflexes using the linear model (−0.43 ± 0.13 predicted vs. −0.41 ± 0.10 measured). We conclude that the linear model can be used as the first approximation to interpret AP response during neck suction.

Overall open-loop gain of rapidly acting arterial pressure control system in rabbits

1983 ◽  
Vol 399 (2) ◽  
pp. 134-138 ◽  
Author(s):  
Hiroshi Hosomi ◽  
Hiroshi Chatani ◽  
Takaaki Kaizuka ◽  
Shinichiro Katsuda ◽  
Yoshiaki Hayashida
Keyword(s):  
Control System ◽  
Arterial Pressure ◽  
Pressure Control ◽  
Open Loop ◽  
Loop Gain ◽  
Pressure Control System ◽  
Arterial Pressure Control System

Short-term control of cardiovascular function: estimation of control parameters in healthy humans

1996 ◽  
Vol 270 (2) ◽  
pp. H651-H660 ◽  
Author(s):  
K. Toska ◽  
M. Eriksen ◽  
L. Walloe
Keyword(s):  
Mathematical Model ◽  
Arterial Pressure ◽  
Closed Loop ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Open Loop ◽  
Control Parameters ◽  
Short Term ◽  
Model Simulations ◽  
Healthy Humans

In a previous study, we recorded short-term cardiovascular responses after a steep increase in arterial pressure in healthy humans [Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H199-H211, 1994]. The aim of the present study was to develop a mathematical model of the baroreflex control of arterial pressure, to use this model with the previously recorded data to estimate unknown parameters in the reflex control loop, and then to analyze the overall open- and closed-loop performance of the system by model simulations with use of individual sets of optimal parameters. The mathematical model consists of a heart, a linear elastic arterial reservoir, and two parallel resistive vascular beds. The arterial baroreflex loop is modeled by two separate time domain processing objects, each with its own gain, time constant, and delay, to simulate the action of a sympathetic signal to the peripheral vascular bed and a parasympathetic signal to the heart. In repeated model simulations, the control parameters in the model were systematically adjusted by an automated algorithm that minimized the deviations between the time courses of the cardiovascular variables simulated by the model and the previously recorded responses in each individual. In all 10 subjects, the short-term cardiovascular responses were adequately simulated by using individual sets of parameters in the model. Open-loop transfer functions for arterial pressure control were obtained by using the individual sets of optimal model parameters in new simulation runs. Open-loop gain for arterial pressure control at nearly zero frequency (steady state) was between 0.9 and 4. Model simulations also indicated an underdampened response at 0.05-0.07 Hz in the closed-loop situation in four subjects, corresponding to peaks in the mean arterial pressor power spectra obtained from separate recordings of spontaneous variations in the resting situation.

Dexamethasone attenuates the modulatory effect of the insular cortex on the baroreflex in anesthetized rat

2021 ◽  
Author(s):  
Tatiana Sergeevna Tumanova ◽  
Tatiana Nikolaevna Кokurina ◽  
Galina Ivanovna Rybakova ◽  
Viacheslav G. Aleksandrov
Keyword(s):  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Insular Cortex ◽  
Neural Mechanism ◽  
Arterial Baroreflex ◽  
Inhibitory Effects ◽  
Short Term ◽  
Central Autonomic Network

The arterial baroreflex (BR) is an important neural mechanism for the stabilization of arterial pressure (AP). It is known that the insular cortex (IC) and other parts of the central autonomic network (CAN) are able to modulate the BR arc, altering baroreflex sensitivity (BRS). In addition, the sensitivity of the BR changes under the influence of hormones, in particular glucocorticoids (GC). It has been suggested that GC may influence BRS by altering the ability of the IC to modulate the BR. This hypothesis has been tested in experiments on rats anesthetized with urethane. It was found that microelectrostimulation of the visceral area in the left IC causes a short-term drop in AP, which is accompanied by bradycardia, and impairs BRS. The synthetic GC dexamethasone (DEX) did not significantly affect the magnitude of depressor responses but increased BRS and impaired the effect of IC stimulation on the BR. The results obtained confirm the hypothesis put forward and suggest that GC can attenuate the inhibitory effects of the IC on the BR arc, thereby enhancing the sensitivity of the BR.

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