Baroreceptor reflex cardiovascular control in mongrel dogs and racing greyhounds

1985 ◽  
Vol 249 (3) ◽  
pp. H655-H662 ◽  
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw ◽  
D. K. Detweiler
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Open Loop ◽  
Baroreceptor Reflex ◽  
Operating Point ◽  
Baroreflex Control ◽  
Pulsatile Pressure ◽  
Carotid Sinus Baroreflex ◽  
Before And After

The open-loop carotid sinus baroreflex control of arterial pressure-flow relations were compared in mongrel dogs and racing greyhounds (GH) anesthetized with alpha-chloralose. The carotid sinuses were bilaterally isolated and perfused under controlled pressure. Pulsatile pressure and flow were simultaneously measured in the ascending aorta, the celiac, superior mesenteric, left renal, and right iliac arteries. Open-loop set point values of mean arterial pressure were higher in GH before and after vagotomy. Reflex gains were similar before vagotomy but lower in GH after vagotomy. The overall range of control of arterial pressure was the same before vagotomy but smaller in GH after vagotomy. The variation of mean arterial pressure with mean carotid sinus pressure in GH was shifted toward higher pressure levels similar to resetting. The overall effects of vagotomy on carotid sinus baroreceptor reflex responses were smaller in GH. Operating point values of regional resistance were generally smaller in GH. Operating point sensitivities of regional resistance were the same except for the iliac bed, which was more sensitive in GH. These results document significant regional differences in the baroreceptor control of regional hemodynamics between mongrels and greyhounds that could contribute to altered responses especially to "hypertensive" perturbations.

Effects of anesthesia on carotid sinus reflex control of arterial hemodynamics in the dog

1980 ◽  
Vol 239 (5) ◽  
pp. H681-H691 ◽  
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Operating Point ◽  
Set Point ◽  
Arterial Hemodynamics ◽  
Pulsatile Pressure ◽  
Reflex Gain ◽  
Reflex Control

The detailed characteristics of the carotid sinus reflex control of regional pressure-flow relations were compared in dogs anesthetized with chloralose, pentobarbital, or halothane. The carotid sinuses were isolated and perfused under conditions of controlled pulsatile pressure. Pressure and flow were measured in the ascending aorta and the celiac, mesenteric, renal, and iliac artery. Mean arterial pressure and peripheral resistance were highest under chloralose and lowest under halothane. For cardiac output this relation was reversed. Set point values of reflex gain and overall range of control were similar under chloralose and halothane and lowest under pentobarbital. These results were found both before and after bilateral cervical vagotomy. Operating point values of regional resistance were generally largest with chloralose and smallest with halothane. Operating point sensitivities of regional resistances were generally smallest under pentobarbital and similar under chloralose and halothane. Vagotomy was associated with increases in set point values of mean arterial pressure, set point gain, and overall range of control under all three anesthetics. With chloralose as a reference, halothane does not depress cardiovascular reflex mechanisms. Carotid sinus reflexes under halothane were as sensitive and well maintained as they were under chloralose. These reflexes were significantly depressed under pentobarbital compared with chloralose.

Sinovagal interaction in arterial pressure restoration after 10% hemorrhage

1979 ◽  
Vol 237 (3) ◽  
pp. R203-R209 ◽  
Author(s):  
H. Hosomi ◽  
K. Sagawa
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressure Measurement ◽  
Carotid Sinus ◽  
Open Loop ◽  
Baroreceptor Reflex ◽  
Conscious Dogs ◽  
Intact Condition ◽  
Reflex System ◽  
Additive Summation

The summation between the carotid sinus baroreceptor reflex system (CS system) and the vagally mediated reflex system (V system) was studied as they restore mean arterial pressure (MAP) after 10% quick hemorrhage in splenectomized conscious dogs chronically instrumented with catheters for pressure measurement and hemorrhage. The experiment was repeated under nerve-intact condition (intact), with cold block of the vagi ([V]), after carotid sinus denervation (CS), and CS plus [V] situations. MAP falls at 1.5 min after the hemorrhage were 7.2 in intact, 24.7 in [V], 36.0 in CS, and 67.6 in CS + [V] mmHg. When we calculated the open-loop gains of CS and V systems assuming a simply additive summation between them a self-contradiction occurred. To avoid this contradiction, it was necessary to assume that CS and V systems interact in a facilitatory manner. Mean open-loop gains calculated under this assumption were 1.64 for the CS system alone, 0.89 for the V system alone, and 6.59 for the interacting component between them. These intriguing results warrant further analysis of the summation between the two reflex systems.

Pulsatile vs. mean component of baroreflex compensation for posthemorrhage hypotension

1988 ◽  
Vol 254 (6) ◽  
pp. H1074-H1080
Author(s):  
T. Yamazaki ◽  
M. J. Brunner ◽  
K. Sagawa
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Aortic Pressure ◽  
Open Loop ◽  
Feedback Condition ◽  
Carotid Baroreflex ◽  
Pulsatile Pressure ◽  
Mean Pressure ◽  
Pressure Feedback

We studied the influence of pulsatile pressure and mean arterial pressure signals on the restoration of arterial pressure after 10% hemorrhage in seven anesthetized dogs. After transection of the aortic nerve, a quick 10% hemorrhage was repeated under four different sinus conditions: condition 1, carotid sinus pressure depulsated and fixed at a level equal to the prehemorrhage level (no feedback); condition 2, pulsatile component of aortic pressure fed back to the carotid sinus with a fixed mean pressure (pulsatile feedback); condition 3, depulsated mean aortic pressure fed back (mean pressure feedback); condition 4, both pulsatile and mean pressure fed back (pulsatile plus mean component feedback). The restoration of arterial pressure in condition 2 was not significantly different from that in condition 1, but there was greater restoration in conditions 3 and 4. At 1.5 min posthemorrhage, the open-loop gains calculated from the restoration values were nearly zero for the pulsatile feedback only, 2.8 +/- 0.8 for mean arterial pressure feedback, and 1.5 +/- 0.3 for pulsatile and mean pressure feedback. These results indicate that the pulsatile component of the carotid baroreflex contributes minimally to the restoration of arterial pressure after 10% hemorrhage in the anesthetized dog.

Lack of time-dependent augmentation of carotid sinus baroreflex system after vagotomy

1982 ◽  
Vol 242 (4) ◽  
pp. H580-H584
Author(s):  
H. Hosomi ◽  
K. Yokoyama
Keyword(s):  
Control System ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Pressure Control ◽  
Open Loop ◽  
Carotid Sinus Baroreflex ◽  
Stepwise Reduction ◽  
Intact Condition ◽  
Pressure Control System ◽  
Arterial Pressure Control System

The purpose of this experiment was to study whether the carotid sinus baroreflex system (CS system) increases its gain with time after vagotomy in compensation for the loss of the vagally mediated arterial pressure control system (V system). In 7 dogs anesthetized with pentobarbital sodium we determined the responsiveness of the V system by repeatedly measuring the overall open-loop gain (G) of the negative feedback control system. G was assessed as (delta API/delta APS) -- 1, where delta API and delta APS are, respectively, the immediate and steady-state falls in arterial pressure at the aortic arch following a stepwise reduction in blood volume. delta API, delta APS, and G in intact condition were -12.0 +/- 1.8 mmHg, -1.1 +/- 0.2 mmHg, and 10.1 +/- 0.7 (SD), respectively. delta API, delta APS, and G after vagotomy, i.e., G of the CS system (GCS), were -15.6 +/- 3.6 mmHg, -6.4 +/- 1.9 mmHg, and 1.6 +/- 0.4 GCS did not change with time over 4 h after vagotomy. We conclude that the CS system cannot augment its ability to restore arterial pressure in compensation for the lost function of the V system within 4 h after vagotomy in the anesthetized dog.

Baroreflex responsiveness is maintained during isometric exercise in humans

1986 ◽  
Vol 61 (2) ◽  
pp. 797-803 ◽  
Author(s):  
T. J. Ebert
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Maximum Voluntary Contraction ◽  
Transmural Pressure ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Baroreflex Function ◽  
Isometric Handgrip Exercise

The simultaneous rise in heart rate and arterial pressure during isometric handgrip exercise suggests that arterial baroreflex control may be altered. We applied incremental intensities of neck suction and pressure to nine healthy young men to alter carotid sinus transmural pressure. Carotid stimuli were delivered during 1) supine control, 2) “anticipation” of beginning exercise, and 3) handgrip (20% of maximum voluntary contraction). Anticipation was a quiet period, immediately preceding the beginning of handgrip, when no muscular work was being performed. Compared with control, the R-R interval prolongation and mean arterial pressure decline provoked by carotid stimuli were decreased during the anticipation period. These data suggest that influences from higher central neural locations may alter baroreflex function. Furthermore, we derived stimulus-response curves relating carotid sinus transmural pressure to changes in R-R interval and mean arterial pressure. These curves were shifted during handgrip; however, calculated regression slopes were not changed from control. The data indicate that isometric handgrip exercise has a specific influence on human carotid baroreflex control of arterial pressure and heart period: baroreflex function curves are shifted rightward during handgrip, whereas baroreflex sensitivity is unchanged. Furthermore, central neural influences may be partially involved in these alterations.

Baroreflex control of heart interval in conscious renal hypertensive dogs

1981 ◽  
Vol 241 (3) ◽  
pp. H332-H336
Author(s):  
M. D. Thames ◽  
C. L. Eastham ◽  
M. L. Marcus
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Hypertension ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Cholinergic Mechanisms ◽  
Baroreflex Control ◽  
Control Heart ◽  
Before And After ◽  
Autonomic Blockade

The purpose of this study is to determine if baroreflex control of heart interval is abnormal in conscious dogs with renal hypertension. Changes in heart interval in response to transient nitroglycerin-induced decreases in arterial pressure and transient phenylephrine-induced increases in arterial pressure were determined in nine normotensive [mean arterial pressure 92 +/- 4 (SE) mmHg] and nine renal hypertensive conscious dogs (mean arterial pressure 139 +/- 10 mmHg). Data were acquired before and after beta-adrenergic blockade with 2 mg/kg iv propranolol and before and after parasympathetic blockade with 0.5 mg/kg iv atropine. Control heart rates for the normotensive and hypertensive dogs were not different (91 +/- 4 and 93 +/- 7 beats/min, respectively). Before autonomic blockade, the responses of normotensive and hypertensive dogs to nitroglycerin were not different. However, prolongation of the heart interval in response to phenylephrine in hypertensive dogs was significantly less than in normotensive dogs. In both groups, atropine nearly abolished the decrease in heart interval in response to nitroglycerin and the increase in heart interval in response to phenylephrine, although there were small but significant residual responses. Propranolol was without significant effect on heart interval responses to nitroglycerin and phenylephrine. We conclude that the baroreflex control of heart interval during transient decreases in arterial pressure is preserved in hypertensive dogs and is mediated mainly by decreases in parasympathetic outflow to the heart. In contrast, baroreflex control of heart interval during transient increases in arterial pressure is impaired in hypertension and is mediated mainly by activation of parasympathetic cholinergic mechanisms.

scholarly journals Derangement of open-loop static and dynamic characteristics of the carotid sinus baroreflex in streptozotocin-induced type 1 diabetic rats

2018 ◽  
Vol 315 (3) ◽  
pp. R553-R567 ◽  
Author(s):  
Toru Kawada ◽  
Shuji Shimizu ◽  
Yohsuke Hayama ◽  
Hiromi Yamamoto ◽  
Keita Saku ◽  
...  
Keyword(s):  
Dynamic Characteristics ◽  
Carotid Sinus ◽  
Early Stage ◽  
Open Loop ◽  
Operating Point ◽  
Control Group ◽  
Static And Dynamic Characteristics ◽  
Carotid Sinus Baroreflex ◽  
Type 1 Dm

Although diabetes mellitus (DM) is a major risk factor for cardiovascular diseases, changes in open-loop static and dynamic characteristics of the arterial baroreflex in the early phase of DM remain to be clarified. We performed an open-loop systems analysis of the carotid sinus baroreflex in type 1 DM rats 4 to 5 wk after intraperitoneal streptozotocin injection ( n = 9) and we compared the results with control rats ( n = 9). The operating-point baroreflex gain was maintained in the DM rats compared with the control rats (2.07 ± 0.67 vs. 2.66 ± 0.22 mmHg/mmHg, P = 0.666). However, the range of arterial pressure (AP) control was narrower in the DM than in the control group (48.0 ± 5.0 vs. 77.1 ± 4.5 mmHg, P = 0.001), suggesting that the reserve for AP buffering is lost in DM. Although baroreflex dynamic characteristics were relatively preserved, coherences were lower in the DM than in the control group. The decreased coherence in the neural arc may be related to the narrowed quasi-linear range in the static relationship between carotid sinus pressure and sympathetic nerve activity in the DM group. Although the reason for the decreased coherences in the peripheral arc and the total reflex arc was inconclusive, the finding may indicate a loss of integrity of the baroreflex-mediated sympathetic AP control in the DM group. The derangement of the baroreflex dynamic characteristics is progressing occultly in this early stage of type 1 DM in a manner where dynamic gains are relatively preserved around the normal operating point.

Modulation of the baroreceptor reflex by the dorsomedial hypothalamic nucleus and perifornical area

2006 ◽  
Vol 290 (4) ◽  
pp. R1020-R1026 ◽  
Author(s):  
Lachlan M. McDowall ◽  
Jouji Horiuchi ◽  
Suzanne Killinger ◽  
Roger A. L. Dampney
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Psychological Stress ◽  
Cardiovascular Response ◽  
Baroreceptor Reflex ◽  
Hypothalamic Nucleus ◽  
Baroreflex Control ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Renal Sympathetic

Neurons within the dorsomedial hypothalamic nucleus (DMH) and perifornical area (PeF), which lie within the classic hypothalamic defense area, subserve the cardiovascular response to psychological stress. Previous studies have shown that electrical stimulation of the hypothalamic defense area causes inhibition of the cardiac and (in some cases) sympathetic components of the baroreceptor reflex. In contrast, naturally evoked psychological stress does not appear to be associated with such inhibition. In this study, we tested the effect of specific activation of neurons within the DMH and PeF on the baroreflex control of renal sympathetic nerve activity and heart rate in urethane-anesthetized rats. Microinjection of bicuculline (a GABAA receptor antagonist) into the DMH caused dose-dependent increases in heart rate and renal sympathetic activity, shifted the baroreflex control of both variables to higher levels (i.e., increased the upper and lower plateaus of the baroreflex function curves, and increased the threshold, midpoint, and saturation levels of mean arterial pressure). The maximum gain of the sympathetic component of the baroreflex was also increased, while that of the cardiac component was not significantly changed. Increases in the midpoint were very similar in magnitude to the evoked increases in baseline mean arterial pressure. Microinjection of bicuculline into the PeF evoked very similar effects. The results indicate that disinhibition of neurons in the DMH/PeF region not only increases sympathetic vasomotor activity and heart rate but also resets the baroreceptor reflex such that it remains effective, without any decrease in sensitivity, over a higher operating range of arterial pressure.

Carotid sinus baroreflex control of beta-endorphin release in anesthetized dogs

1989 ◽  
Vol 256 (2) ◽  
pp. R408-R412
Author(s):  
M. J. Brunner ◽  
K. E. Wehberg ◽  
J. C. Williams ◽  
C. A. Cahill
Keyword(s):  
Carotid Sinus ◽  
Venous Blood ◽  
Normal Component ◽  
Vagal Afferents ◽  
Mixed Venous Blood ◽  
Baroreflex Control ◽  
Beta Endorphin ◽  
Carotid Sinus Baroreflex ◽  
Before And After ◽  
Anesthetized Dogs

A quantitative assessment of the carotid sinus baroreflex release of endogenous plasma beta-endorphin-like immunoreactive material has been established. The carotid sinuses of 12 pentobarbital sodium-anesthetized dogs were isolated bilaterally and perfused with a constant pressure maintained by infusion or withdrawal of normal saline. Mean arterial pressure (MAP) and heart rate (HR) were monitored. Carotid sinus pressure (CSP) was changed from 200 to 50 mmHg in 25 mmHg steps before and after vagotomy. At each interval of CSP, 10 ml mixed venous blood were collected, and beta-endorphin-like peptides were extracted from plasma and assayed. Concentrations of plasma beta-endorphin-like material were determined by radioimmunoassay. Sigmoidal responses of MAP and HR were revealed during changes in CSP. No significant differences in beta-endorphin-like immunoreactivity (beta-END-L-I) were measured at CSP of 200 and 50 in the intact condition (35.9 +/- 3.9 and 35.0 +/- 6.4 fm/ml, respectively). However, after vagotomy, beta-END-L-I measured at 50 mmHg CSP was significantly elevated to 53.3 +/- 5.2 fm/ml compared with the value of 35.5 +/- 7.2 fm/ml at CSP of 200 mmHg. The results suggest that the release of beta-endorphin is modulated by the action of the carotid baroreflex as a normal component of an integrated efferent response. However, this response is normally buffered by reflexes with vagal afferents.

Role of carotid sinus baroreflex in attenuating systemic arterial pressure variability studied in anesthetized dogs

1994 ◽  
Vol 266 (2) ◽  
pp. H720-H729 ◽  
Author(s):  
T. Yoshida ◽  
Y. Harasawa ◽  
T. Kubota ◽  
H. Chishaki ◽  
T. Kubo ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Amplitude Spectrum ◽  
Low Frequency ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Frequency Range ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs

Attenuation of systemic arterial pressure (SAP) variability by the carotid sinus baroreflex (CSBR) was quantified in nine anesthetized, vagotomized dogs. SAP amplitude spectrum was compared between open-loop [SAPo(f)] and closed-loop [SAPc(f)] operation of the CSBR. At 0.002 Hz, SAPc amplitude was 3.5 +/- 2.2 (SD) mmHg, and SAPo was 9.6 +/- 3.5 mmHg (P < 0.01). At 0.02 Hz, SAP(c) amplitude was 2.8 +/- 1.2 mmHg, and SAPo was 4.3 +/- 1.2 mmHg (P < 0.05). At higher frequencies, SAPo(f) was indistinguishable from SAPc(f). With the opened CSBR, intracarotid sinus pressure (CSP) was pseudorandomly varied, and the resulting SAP responses were recorded to determine the transfer function from CSP to SAP [HCSP.SAP(f)]. From SAPo(f) and the determined HCSP.SAP(f), we estimated SAP(f) if the CSBR was closed [SAPc,est(f)] and compared it with SAPc(f). These two spectra were similar in each dog over a frequency range of 0.002–0.15 Hz, the differences between SAPo(f) and SAPc(f) being reconcilable with HCSP.SAP(f). Although the anesthetized state and vagotomy may have distorted the transfer characteristics of the CSBR from those in conscious (with the intact vagi) states, the results of the present study indicate that the CSBR attenuated SAP variability mainly in a low-frequency range below 0.02 Hz and that this attenuation was attributable to the transfer properties of the CSBR.

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