Servoanalysis of Carotid Sinus Reflex Effects on Peripheral Resistance

Scher, Allen M.; Young, Allan C.

doi:10.1161/01.res.12.2.152

Cited by 168 publications

(63 citation statements)

References 13 publications

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“…∆AP I is observed in animals whose AP feedback baroreflex control system has been completely eliminated [9]. The baroreflex system operates at least about 2 sec after the application of external disturbances, such as hemorrhage, to the system [20]. Immediately after the rapid mild hemorrhage, the baroreflex system does not function [20].…”

Section: Discussionmentioning

confidence: 99%

“…The baroreflex system operates at least about 2 sec after the application of external disturbances, such as hemorrhage, to the system [20]. Immediately after the rapid mild hemorrhage, the baroreflex system does not function [20]. These facts suggest that ∆AP I is in major part determined by cardiovascular mechanical properties, such as distensibility of the aortic wall, capacity of the aorta, rate of filling the aorta with blood, rate of draining blood from the aorta to the peripheral vessels, and so forth.…”

Section: Discussionmentioning

confidence: 99%

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Time-Dependent Change in Baroreflex Control Capacity of Arterial Pressure by Pentobarbital Anesthesia in Rabbits.

et al. 2000

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Abstract:The present study is designed to investigate the time-dependent effect of pentobarbital anesthesia on the baroreflex arterial pressure (AP) control system in rabbits. The overall AP control capacity of the baroreflex system was assessed with mean arterial pressure (MAP) responses to the rapid mild hemorrhage (2 ml/kg body weight) and an overall open-loop gain (G) of the system. The G value was determined by means of the following formula: G=∆AP I /∆AP S -1, where ∆AP I is an immediate MAP fall and ∆AP S a steady-state fall after the rapid hemorrhage. Prior to the experiment, two catheters for AP measurement and hemorrhage were chronically in-dwelt in the aortic arch via the left subclavian and left common carotid arteries, respectively. Control mean arterial pressure averaged for 30 sec before the rapid hemorrhage (CMAP), ∆AP I and ∆AP S significantly increased and reached the maximal value at 14 min (CAMP: p<0.01) and 28 min (∆AP I : p<0.01 and ∆AP S : p<0.01) after the intravenous injection of sodium pentobarbital in a 25.0 mg/kg dose, respectively. These values gradually decreased in the course of time and tended to recover to near the preanesthetic level at 77-98 min after the anesthesia. The G value significantly decreased from 7.3 in the conscious state to 1.5 at 28 min after the anesthesia (p<0.001), gradually increased with lapse of time and recovered to near the preanesthetic level at 77-98 min after the anesthesia. No significant difference in G was observed between in the conscious and anesthetized states beyond 70 min after the anesthesia (p>0.05). These findings suggest that pentobarbital sodium exerts a timedependent inhibitory effect on the baroreflex system but does not significantly affect the overall AP control capacity of the baroreflex system itself at least 70 min after the intravenous administration at a dose of 25.0 mg/kg.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Time-Dependent Change in Baroreflex Control Capacity of Arterial Pressure by Pentobarbital Anesthesia in Rabbits.

et al. 2000

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“…1 need not be questioned. Whether the feedback is a simple proportional control or not remains to be answered, but it has been shown that it behaves as such in experimental animals (Sher and Young 1963;Schmidt et al 1972). The adaptation of the baroreceptor is known, which indicates that it partly has a characteristic of derivative control.…”

Section: Fig 2 Andmentioning

confidence: 99%

“…A search for the literature revealed a good deal of information and analysis along this line in animal experiments (Sagawa et al 1962;Sagawa 1967;Sher et al 1963;Hatakeyama 1967;Schmidt et al 1971). While the vasomotor waves in man have seldom, if ever, been reported, the information on the gain and the signal delay of the feedback loop in man, which controls the arterial pressure, is unobtain able.…”

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confidence: 99%

Analysis of the Vasomotor Waves Observed during Cardiopulmonary Bypass

Suwa

Yamamura

1980

Tohoku J. Exp. Med.

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From the data of the vasomotor waves (VMW) previously reported, we attempted to retrieve information of the gain and the dead-time of the feedback circuit involved.A mathematical analysis revealed a certain relationship between the gain and the dead-time for the VMW to occur in three models. Combining our result with the data of animal experiments obtained by other researchers, we could exclude one of three models, thereby setting the area of existence of gain-delay value. When we apply a value of 3.4 sec for dead-time, as extrapolated from the animal data, the static gain of the system is between 2.2 and 4.0. Contrary to those observed in animal experiments and to our own original speculation, the VMW in man during cardiopulmonary bypass is likely caused via baroreceptor (carotid sinus) reflex rather than through cerebral ischemic response. ---vasomotor waves; blood pressure control; feedback gain; dead time; baroreceptor reflex In a previous paper, we described slow sinusoid variation of arterial pressure (the vasomotor waves: the VMW ), which occurred in several cases during cardio pulmonary bypass (Suwa and Asahara 1978). When we first observed this phenomenon, we intuitively felt that, by analyzing these waves, we may be able to obtain information about the gain and signal delay of the feedback system which controls the arterial pressure.

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“…Furthermore, we found few studies related to quantification of the dynamic properties of the TPR baroreflex (e.g., the time course TPR takes to reach its steady-state value in response to step excitation), perhaps due to the inability to measure sufficiently rapid TPR changes in which Ohm's law may no longer be valid as well as the enhanced demands on experimentation and/or data analysis. In earlier studies, Rosenbaum et al and other investigators (5,25,26) experimentally maintained flow or pressure to a particular regional circulation so as to measure peripheral resistance changes through pressure or flow at that region and then quantified the dynamic properties of one baroreflex by applying step excitation, sinusoidal stimulations at various frequencies, or randomized perturbation in conjunction with system identification analysis of the measured variations. However, this approach is obviously difficult and not as relevant to overall ABP regulation as those studies that have observed TPR.…”

mentioning

confidence: 99%

Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability

Chen

Kim²,

Sala‐Mercado³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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DS, Mukkamala R. Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability. Am J Physiol Heart Circ Physiol 294: H293-H301, 2008. First published November 2, 2007 doi:10.1152/ajpheart.00852.2007.-We previously developed a mathematical analysis technique for estimating the static gain values of the arterial total peripheral resistance (TPR) baroreflex (GA) and the cardiopulmonary TPR baroreflex (GC) from small, spontaneous beat-to-beat fluctuations in arterial blood pressure, cardiac output, and stroke volume. Here, we extended the mathematical analysis so as to also estimate the entire arterial TPR baroreflex impulse response [hA(t)] as well as the lumped arterial compliance (AC). The extended technique may therefore provide a linear dynamic characterization of TPR baroreflex systems during normal physiological conditions from potentially noninvasive measurements. We theoretically evaluated the technique with respect to realistic spontaneous hemodynamic variability generated by a cardiovascular simulator with known system properties. Our results showed that the technique reliably estimated hA(t) [error ϭ 30.2 Ϯ 2.6% for the square root of energy (EA), 19.7 Ϯ 1.6% for absolute peak amplitude (PA), 37.3 Ϯ 2.5% for GA, and 33.1 Ϯ 4.9% for the overall time constant] and AC (error ϭ 17.6 Ϯ 4.2%) under various simulator parameter values and reliably tracked changes in GC. We also experimentally evaluated the technique with respect to spontaneous hemodynamic variability measured from seven conscious dogs before and after chronic arterial baroreceptor denervation. Our results showed that the technique correctly predicted the abolishment of hA (t) , and GA ϭ Ϫ2.1 Ϯ 0.6 to 0.3 Ϯ 0.2 (P Ͻ 0.05)] and the enhancement of GC [Ϫ0.7 Ϯ 0.44 to Ϫ1.8 Ϯ 0.2 (P Ͻ 0.05)] following the chronic intervention. Moreover, the technique yielded estimates whose values were consistent with those reported with more invasive and/or experimentally difficult methods. autonomic nervous system; hemodynamics; modeling; system identification; transfer function THE TOTAL PERIPHERAL RESISTANCE (TPR) baroreflex is a wellappreciated feedback control mechanism for rapid arterial blood pressure (ABP) regulation. Consistent with negative feedback, the arterial TPR baroreflex is widely known to respond to a step increase (decrease) in ABP by decreasing (increasing) steady-state TPR. Similarly, the cardiopulmonary TPR baroreflex has been shown to respond to a step increase (decrease) in central venous pressure (CVP) by decreasing (increasing) steady-state TPR (24). In this way, the cardiopulmonary TPR baroreflex is able to anticipate and thereby quickly buffer the imminent change in ABP that will arise from the preload alteration.Much of our knowledge of the TPR baroreflex systems is owed to open-loop studies in which the steady-state or static gain properties of one baroreflex was experimentally determined by selectively exciting it and measuring the steady-state TPR response via Ohm's law [i.e., ABP ...

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Servoanalysis of Carotid Sinus Reflex Effects on Peripheral Resistance

Cited by 168 publications

References 13 publications

Time-Dependent Change in Baroreflex Control Capacity of Arterial Pressure by Pentobarbital Anesthesia in Rabbits.

Time-Dependent Change in Baroreflex Control Capacity of Arterial Pressure by Pentobarbital Anesthesia in Rabbits.

Analysis of the Vasomotor Waves Observed during Cardiopulmonary Bypass

Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability

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