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J Appl Physiol 89: 1979-1984, 2000;
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Vol. 89, Issue 5, 1979-1984, November 2000

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

Toru Kawada, Masashi Inagaki, Hiroshi Takaki, Takayuki Sato, Toshiaki Shishido, Teiji Tatewaki, Yusuke Yanagiya, Masaru Sugimachi, and Kenji Sunagawa

Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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.

systems analysis; closed-loop gain; open-loop gain; rabbits


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

NECK SUCTION PROCEDURES have been widely used in the evaluation of carotid sinus baroreflex function in humans (6-9, 17, 18, 24). During neck suction, a negative pressure is applied around the neck to activate the carotid sinus baroreflex, resulting in a decrease in arterial pressure (AP). Because decreased AP deactivates the aortic baroreceptors, negative feedback through the aortic baroreflex operates to increase AP, thereby counteracting the carotid sinus baroreflex during neck suction. To avoid the counteracting effect of the aortic baroreflex during neck suction, the initial heart rate response before the beginning of AP response has been used to evaluate the carotid sinus baroreflex function (6-9, 24, 26). However, the initial heart rate response alone cannot account for the total buffering effect of carotid sinus baroreflex against pressure perturbation. A quantitative analysis of the AP response is crucial to extend the interpretation of observed AP response during neck suction. However, to the best of our knowledge, no efforts have been made to quantify the counteraction of the aortic baroreflex to the carotid sinus baroreflex during neck suction. This is possibly because respective evaluations of the carotid sinus and aortic baroreflexes are impossible in human study. Although a simple linear model can be put forward to explain the counteraction of the aortic baroreflex to the carotid sinus baroreflex during neck suction, the presence of interactions between the carotid sinus and aortic baroreflexes (3, 12, 15, 25, 27) may complicate the AP response. To test the hypothesis that the AP response during neck suction can be explained by the linear model, 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 the present animal model, we enabled or disabled the aortic baroreflex to measure counteraction of the aortic baroreflex to the carotid sinus baroreflex.


    MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Theoretical Considerations

Were it not for the aortic baroreflex, pressure changes associated with a given neck suction procedure could be described by the block diagram shown in Fig. 1A (20). Delta AP indicates changes in AP during neck suction. GCS indicates the open-loop gain of the carotid sinus baroreflex. We defined GCS as a positive value for convenience and added a negative sign to GCS to indicate the negative feedback through the carotid sinus baroreflex. Delta X represents a pressure perturbation during neck suction. As an example, a neck suction of 50 mmHg corresponds to a Delta X of 50 mmHg. Under these conditions, the closed-loop gain during neck suction (GNS), defined as the ratio of Delta AP to Delta X, is
G<SUB>NS</SUB><IT>=</IT><FR><NU><IT>&Dgr;</IT>AP</NU><DE>&Dgr;X</DE></FR><IT>=</IT>−<FR><NU>G<SUB>CS</SUB></NU><DE><IT>1+</IT>G<SUB>CS</SUB></DE></FR> (1)
As indicated in Eq. 1, GNS has a negative value and asymptotically approaches -1 as GCS increases. Rearranging Eq. 1 for GCS yields
G<SUB>CS</SUB><IT>=</IT>−<FR><NU>G<SUB>NS</SUB></NU><DE><IT>1+</IT>G<SUB>NS</SUB></DE></FR> (2)
Shubrooks (23) adopted Eq. 2 to estimate GCS during neck suction in anesthetized dogs.


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  		Fig. 1.   Block diagrams showing arterial pressure control during neck suction without (A) and with (B) the aortic baroreflex. Delta X, a pressure perturbation; Delta AP, the arterial pressure response; GCS, open-loop gain of the carotid sinus baroreflex; GAO, open-loop gain of the aortic baroreflex.

When the aortic baroreflex is taken into account, pressure changes during the neck suction procedure can be described by using the block diagram shown in Fig. 1B. GAO indicates the open-loop gain of the aortic baroreflex. We assigned GAO a positive value for convenience and added a negative sign to GAO to describe the negative feedback through the aortic baroreflex. Under these conditions, GNS is
G<SUB>NS</SUB><IT>=</IT><FR><NU><IT>&Dgr;</IT>AP</NU><DE>&Dgr;X</DE></FR><IT>=</IT>−<FR><NU>G<SUB>CS</SUB></NU><DE><IT>1+</IT>G<SUB>CS</SUB><IT>+</IT>G<SUB>AO</SUB></DE></FR> (3)
As indicated in Eq. 3, GNS has a negative value and asymptotically approaches -1 as GCS increases. In addition, GNS asymptotically approaches zero as GAO increases.

Surgical Preparation

Animal care was in accordance with the Guiding Principles for the Care and Use of Animals in the Field of Physiological Sciences approved by the Physiological Society of Japan. Six Japanese white rabbits weighing between 2.4 and 3.1 kg were anesthetized via intravenous injection (2 ml/kg) of a mixture of urethane (250 mg/ml) and alpha -chloralose (40 mg/ml) and mechanically ventilated with oxygen-enriched room air. Supplemental anesthetics were injected as necessary (0.5 ml/kg) to maintain an appropriate depth of anesthesia. AP was recorded through a catheter inserted via the right femoral artery. We vascularly isolated the right carotid sinus from the systemic circulation by ligating the internal and external carotid arteries as well as other small branches originating from the carotid sinus region. The isolated carotid sinus was flushed and then filled with warmed physiological saline. The intracarotid sinus pressure (CSP) was controlled through a catheter inserted from the common carotid artery by a servo-controlled piston pump. We also vascularly isolated the baroreceptor regions of the right aortic depressor nerve near the bifurcation of the right common carotid and subclavian arteries via a midline thoracotomy (22). The intracarotid arterial pressure (CAP) was controlled by a second servo-controlled piston pump. The bilateral vagi were cut to eliminate baroreflexes from cardiopulmonary regions. The right vagal nerve was cut intrathoracically to avoid any injury to the right aortic depressor nerve. The remaining carotid sinus and aortic baroreflexes from the left side were interrupted by sinoaortic denervation. Body temperature was maintained at 38°C by using a heating pad.

Protocols

After completion of the surgical preparation, both CSP and CAP were matched to AP, and an equilibrium pressure was obtained. The study consisted of the following three protocols.

Protocol 1. We fixed CAP at the equilibrium pressure throughout the protocol, thereby disabling the aortic baroreflex in response to changes in AP. After AP reached a steady state, we increased CSP above AP by either 30 or 50 mmHg for 60 s to simulate a neck suction procedure. Because the negative pressure is attenuated to 64% from neck to perivascular tissue around the carotid sinus in humans (17), the 30- and 50-mmHg pressure perturbations corresponded to negative pressures of 47 and 78 mmHg around the neck, respectively. The magnitude of pressure perturbation, therefore, should cover the range of the neck suction procedure used in humans.

Protocol 2. To elucidate the counteraction of the aortic baroreflex to the carotid sinus baroreflex, we servo-controlled CAP to follow changes in AP, thereby enabling the aortic baroreflex. After AP reached a steady state, we increased CSP above AP by either 30 or 50 mmHg for 60 s.

Protocol 3. To estimate the aortic baroreflex function alone, we fixed CSP at the equilibrium pressure, thereby disabling the carotid sinus baroreflex in response to changes in AP. After AP reached a steady state, we increased CAP above AP by either 30 or 50 mmHg for 60 s.

The order of protocols was randomized among animals to reduce the likelihood of bias or systematic error in estimating the baroreflex gains. We recorded CSP, CAP, and AP at a sampling rate of 200 Hz using a 12-bit analog-to-digital converter. The data were stored on the hard disk of a dedicated laboratory computer system for subsequent analysis.

Data Analysis

All data are presented as means ± SD. The steady-state AP decrease in each protocol was calculated as the difference between the steady-state and baseline AP values. Baseline AP was obtained by averaging instantaneous AP for 10 s before the pressure perturbation. Steady-state AP was calculated by averaging instantaneous AP for the last 10 s of the 60-s pressure perturbation. We repeated the 60-s pressure perturbation twice in each protocol and represented the steady-state AP decrease as the mean of the two experimental runs.

We examined the differences in steady-state AP decrease between protocols 1 and 2 using a paired t-test (10). The difference was considered statistically significant when P < 0.05. All statistical analyses were performed separately on the results associated with the 30- and 50-mmHg pressure perturbations, because the number of samples would be small for a two-way analysis of variance.

To determine whether Eq. 3 can account for the results of protocol 2, we first calculated GCS from the results of protocol 1 using Eq. 2. We also estimated GAO from the results of protocol 3 by substituting GAO for GCS in Eq. 2. After obtaining GCS and GAO values, we predicted GNS according to the right term of Eq. 3. Finally, we compared the predicted GNS with actual, measured GNS in protocol 2 by using a paired t-test (10).


    RESULTS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Figure 2A shows typical recordings of CSP, CAP, and AP obtained from protocol 1 with a 50-mmHg pressure perturbation. CSP was matched to mean AP in the first 40 s. We then elevated CSP above mean AP by 50 mmHg in the following 60 s. AP decreased in response to the pressure perturbation. Because the pressure difference between CSP and mean AP was kept at 50 mmHg to simulate the neck suction procedure, the decrease in AP caused an overshoot-like change in the CSP tracing. When the 60-s pressure perturbation was discontinued, CSP was again matched to mean AP. The increase in AP upon cessation of pressure perturbation caused a negative overshoot-like change in the CSP tracing. Throughout the protocol, CAP was maintained at the equilibrium pressure to disable the aortic baroreflex in response to any change in AP.


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  		Fig. 2.   Representative recordings of carotid sinus pressure (CSP), carotid arterial pressure (CAP), and systemic arterial pressure (AP) during a 50-mmHg pressure perturbation on CSP. The aortic baroreflex was disabled (A) and enabled (B).

Figure 2B shows typical recordings of CSP, CAP, and AP obtained from protocol 2 with a 50-mmHg pressure perturbation. CSP was controlled in the same manner as in protocol 1. The pressure difference between CSP and mean AP was maintained at 50 mmHg during the 60-s simulated neck suction. In contrast to protocol 1, however, CAP was servo-controlled to follow changes in mean AP, thereby enabling the aortic baroreflex. The steady-state AP decrease was attenuated compared with that in Fig. 2A.

Table 1 summarizes the steady-state AP decreases during the simulated neck suction obtained from protocols 1 and 2. The steady-state AP decrease in protocol 2 was significantly attenuated compared with that in protocol 1 under conditions of either 30- or 50-mmHg pressure perturbation.

                              
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  		Table 1.   Effects of aortic baroreflex on the steady-state arterial pressure response during simulated neck suction

Figure 3 shows typical recordings of CSP, CAP, and AP obtained from protocol 3 with a 50-mmHg pressure perturbation. CSP was maintained at the equilibrium pressure throughout the protocol. Thus the carotid sinus baroreflex was not operative in response to any change in AP. We matched CAP to mean AP in the first 40 s and then elevated CAP above mean AP by 50 mmHg in the following 60 s. AP decreased in response to the pressure perturbation.


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  		Fig. 3.   Representative recordings of CSP, CAP, and AP during a 50-mmHg pressure perturbation on CAP. The carotid sinus baroreflex was disabled.

Table 2 summarizes gain values obtained from the three protocols. The predicted and measured GNS values did not differ significantly under conditions of either 30- or 50-mmHg pressure perturbation (P = 0.59 and P = 0.83, respectively).

                              
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  		Table 2.   Gain values obtained from the three protocols


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

We have shown that the steady-state AP decrease during a simulated neck suction procedure is attenuated by the aortic baroreflex (Table 1). GNS measured in protocol 2 could be predicted from GCS and GAO by using the right term of Eq. 3 (Table 2), suggesting that the AP response during simulated neck suction can be described by the linear model shown in Fig. 1B.

Counteraction of the Aortic Baroreflex

Although counteraction of the aortic baroreflex to the carotid sinus baroreflex during neck suction has been described (19, 20), a quantitative analysis was required to determine whether the block diagram shown in Fig. 1B can account for AP response during neck suction. As shown in Table 2, GNS measured in protocol 2 was predicted reasonably well from GCS and GAO by using the right term of Eq. 3. These results suggest that the block diagram shown in Fig. 1B is useful as the first approximation to interpret the AP response during neck suction.

The amplitude of pressure perturbation is known to affect GCS due to the sigmoidal input-output relationship of the arterial baroreflex system (3, 16, 21, 22, 27). Although a 50-mmHg pressure perturbation seems to be sufficiently large to fall within the range of sigmoidal nonlinearity, GNS predicted from GCS and GAO using Eq. 3 conformed to the measured GNS, suggesting a linearity in the steady-state AP response during the simulated neck suction. Attenuation of pressure perturbation through the closed-loop feedback may account for the observed linearity as follows. The steady-state input to CSP during the simulated neck suction was not Delta X itself but Delta X + Delta AP, as in Fig. 1. For instance, the steady-state input to CSP in protocol 1 was 22.6 mmHg, on average, when a 50-mmHg pressure perturbation was applied. Therefore, the steady-state input during the simulated neck suction might have been within the linear operating range of the AP regulation.

Clinical Implications

As indicated in Eq. 3, we must specify GAO to determine GCS from observed GNS. The GAO-to-GCS ratio was ~0.6 in the present study. Hosomi et al. (11) reported the GAO-to-GCS ratio of ~0.9 using a quick hemorrhage method in anesthetized rabbits. The GAO-to-GCS ratio has been reported as ~0.5 in anesthetized dogs (2, 3, 5). On the basis of these findings, we specified the GAO-to-GCS ratio variously at 0 (aortic baroreflex disabled), 0.5, 1, and 2, then calculated the relationship between GCS and GNS (Fig. 4A). We also calculated (GCS + GAO) vs. GNS (Fig. 4B). In the simulation, GCS or (GCS + GAO) monotonously increased as GNS approached -1, regardless of the GAO-to-GCS ratio. Therefore, if we repeat the neck suction procedure in the same subject before and after some environmental stress and observe an increase in the negative value of GNS, we can at least conclude that the arterial baroreflex gain has also increased.


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  		Fig. 4.   Relationships between GCS and closed-loop gain during neck suction (GNS; A) and between GCS + GAO and GNS (B) on the basis of Eq. 3. alpha , Ratio of GAO to GCS. Hatched areas indicate most likely ranges of alpha  according to animal experiments.

According to the human study in normal subjects by Mancia et al. (18), the regression coefficient of steady-state changes in mean AP on changes in neck tissue pressure is ~0.41. Using this value, we can estimate GCS to be 2.3 when GCS equals GAO on the basis of Fig. 4A. However, these estimations vary depending on the specified ratio of GAO to GCS. Figure 4 would represent the utility as well as the limitation of the neck suction procedure to estimate the open-loop gain of the arterial baroflex from the steady-state AP response during neck suction.

Limitations

There are several limitations to this study. First, we investigated the carotid sinus and aortic baroreflexes in anesthetized rabbits. Although we chose an anesthetic agent that is minimally suppressive to circulatory regulation, the absolute values of GCS and GAO might have been affected by the anesthesia to some degree. However, we compared the predicted GNS and measured GNS under the same anesthetic conditions, and we believe that the linear model shown in Fig. 1B would explain the steady-state AP response to neck suction, even in the absence of anesthesia.

Second, CSP and CAP were exposed to nonpulsatile pressure. The absolute gain values might have been different had CSP and CAP been exposed to pulsatile pressure (2, 4). Furthermore, we denervated the left carotid sinus nerve while preserving the left internal carotid artery to maintain the blood flow to the brain. Therefore, the possible interaction between the left and right carotid sinus baroreflexes during neck suction (26) was not assessed in the present study.

Third, we cut the vagi to eliminate the possible baroreflex from the cardiopulmonary regions. Consequently, we were unable to evaluate the vagal control of heart rate during the simulated neck suction procedure. Several investigators suggest the advantage of using the heart rate response over the AP response (6-9, 24) to evaluate carotid sinus baroreflex function by neck suction. Future studies with intact vagi are required to examine the counteracting effects of the aortic baroreflex on the heart rate response during neck suction.

Finally, we filled the isolated baroreceptor regions with warmed physiological saline (13, 14, 21, 22). Because ion content affects the sensitivity of baroreceptors (1), the absolute values of GCS and GAO might have been different had we used other solutions, such as Ringers solution. However, because we did not change the intravascular content of the isolated baroreceptor regions among protocols, the sensitivity of baroreceptors to pressure input would have remained unchanged.

In conclusion, the aortic baroreflex counteracted the carotid sinus baroreflex during simulated neck suction and attenuated the steady-state AP response. The linear model shown in Fig. 1B was able to account for the AP response during the simulated neck suction. Therefore, we can estimate the arterial baroreflex gain from the observed AP response during neck suction by assuming the GAO-to-GCS ratio. Although the GAO-to-GCS ratio in humans is unknown, according to animal experiments, it most likely falls within the range of 0.5-1.0.


    ACKNOWLEDGEMENTS

This study was supported by Research Grants for Cardiovascular Diseases (9C-1, 11C-3, 11C-7) from the Ministry of Health and Welfare of Japan, by a Health Sciences Research Grant for Advanced Medical Technology from the Ministry of Health and Welfare of Japan, by Special Funds for Encouragement System of COE from the Science and Technology Agency of Japan, by a Ground-Based Research Grant for the Space Utilization promoted by National Space Development Agency of Japan and Japan Space Forum, by a Bilateral International Joint Research Grant from the Science and Technology Agency of Japan, by Grants-in-Aid for Scientific Research (B-11694337, C-11680862, C-11670730), by Grants-in-Aid for the Encouragement of Young Scientists (11770390, 11770391), and by a grant provided by the Ichiro Kanehara Foundation.


    FOOTNOTES

Address for reprint requests and other correspondence: T. Kawada, Dept. of Cardiovascular Dynamics, National Cardiovascular Center Research Inst., 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan (E-mail: torukawa{at}res.ncvc.go.jp).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 7 April 2000; accepted in final form 21 June 2000.


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ABSTRACT
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MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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J APPL PHYSIOL 89(5):1979-1984
8750-7587/00 $5.00 Copyright © 2000 the American Physiological Society


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