Aortic arch reflex control of total systemic vascular capacity

1987 ◽  
Vol 253 (3) ◽  
pp. H598-H603
Author(s):  
A. A. Shoukas ◽  
M. J. Brunner ◽  
A. S. Greene ◽  
C. L. MacAnespie
Keyword(s):  
Arterial Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Reservoir Volume ◽  
Aortic Arch Pressure ◽  
Pressure Changes ◽  
Change In Mean ◽  
Sinus Pressure

The ability of the aortic arch baroreceptors to change vascular capacity was measured and, in the same animal, compared with carotid sinus reflex changes in capacity. Seven dogs were anesthetized with pentobarbital sodium and perfused with constant flow. Changes in external reservoir volume reflected reciprocal changes in total systemic vascular capacity and changes in arterial pressure parallel changes in total peripheral resistance. The aortic arch and carotid sinus baroreceptor areas were isolated, and the pressures were controlled separately. With carotid sinus pressure held constant at 125 mmHg, aortic arch pressure was increased and decreased between 225 and 50 mmHg, and the changes in reservoir volume and systemic arterial pressure were measured. Results from increasing and decreasing aortic arch or carotid sinus pressure were not significantly different and were averaged. The mean change in reservoir volume was 1.9 +/- 0.2 ml/kg and the change in mean arterial pressure was 18.7 +/- 3.7 mmHg. The changes in reservoir volume and arterial pressure caused by the aortic arch reflex were not influenced by the level of carotid sinus pressure. Carotid sinus pressure changes between 200 and 50 mmHg at a constant aortic arch pressure caused reservoir volume and arterial pressure to change by 7.2 +/- 0.9 ml/kg and 45.1 +/- 4.1 mmHg, respectively. The level of aortic arch pressure did not modify these responses.

Effect of cervical sympathetic nerve stimulation on canine carotid sinus reflex

1976 ◽  
Vol 230 (4) ◽  
pp. 1026-1030 ◽  
Author(s):  
CP Bolter ◽  
Ledsome
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Carotid Sinus ◽  
Full Range ◽  
Systemic Arterial Pressure ◽  
Reflex Response ◽  
Cervical Sympathetic ◽  
Pressure Changes ◽  
Cervical Sympathetic Nerve ◽  
Sinus Pressure

In the chloralose-anesthetized dog the carotid sinus on one side of the neck was isolated vascularly. Pressure in the isolated sinus [carotid sinus pressure (CSP)], electrocardiogram, and systemic arterial pressure were recorded. Both vagosympathetic trunks were cut and the contralateral common carotid artery was occluded or the contralateral sinus nerve was cut to reduce reflex buffering of arterial pressure changes. By varying CSP from 50 to 250 mmHg the full range of the reflex response was examined. Electrical stimulation of the peripheral end of the cut ipsilateral cervical sympathetic nerve brought about a rapid decrease in mean arterial pressure (MAP) and heart rate (HR) at lower CSPs, no change in these variables at midrange CSPs, and a gradual increase at higher CSPs, such that the gain of the reflex was reduced (1.89 +/- 0.19 to 1.33 +/- 0.15 mmHg/mmHg). The decrease in MAP and HR at lower CSPs implies an increase in baroreceptor activity whereas the converse would appear to occur at higher CSPs. These responses attained a maximum value at low stimulus frequencies (less than 10 Hz).

Pulsatile sinus pressure changes evoke sustained baroreflex responses in awake dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H673-H678 ◽  
Author(s):  
D. Mendelowitz ◽  
A. M. Scher
Keyword(s):  
Arterial Pressure ◽  
Pulse Pressure ◽  
Carotid Sinus ◽  
Pressure Change ◽  
Conscious Dogs ◽  
Reflex Responses ◽  
Depressor Response ◽  
Pulsatile Pressure ◽  
Pressure Changes ◽  
Sinus Pressure

A modified Stephenson-Donald preparation was used to control pressure in an isolated carotid sinus in conscious dogs with all other arterial baroreceptors denervated. Sinus pressure was changed from preisolation control levels to either an elevated static or an elevated pulsatile pressure for 5 min. These sinus pressure changes evoked similar initial decreases in arterial pressure. The elevated static sinus pressure (150 or 175 mmHg) caused an initial depressor response of -32.7 +/- 5.5 mmHg, which then decayed rapidly. Five minutes after the change in sinus pressure, the depressor response was abolished, as arterial pressure returned to control pressure. This decay of the response would be expected if resetting occurred. In contrast, when the sinus was exposed to elevated pulsatile pressures (125 or 150 mmHg mean, 50 mmHg pulse pressure) depressor responses were sustained throughout the sinus pressure change (-23.2 +/- 5.3 mmHg initial, -29.0 +/- 4.8 mmHg at 5 min; P greater than 0.4). These results demonstrate that while the reflex responses rapidly reset to elevated static sinus pressures, elevated pulsatile pressures elicit sustained reflex responses.

Rabbit carotid sinus reflex under pentobarbital, urethan, and chloralose anesthesia

1984 ◽  
Vol 246 (5) ◽  
pp. H696-H701 ◽  
Author(s):  
N. Ishikawa ◽  
C. H. Kallman ◽  
K. Sagawa
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Logistic Function ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Specific Effects ◽  
Reflex Control ◽  
Alpha Chloralose ◽  
Sinus Pressure

To determine the effects of different anesthesias on the performance of the arterial baro-reflex, the open-loop characteristic of the carotid sinus reflex was analyzed in 24 rabbits under anesthesia with pentobarbital (30 mg/kg), urethan (800 mg/kg), alpha-chloralose (80 mg/kg), or a mixture of alpha-chloralose (40 mg/kg) and urethan (0.4 g/kg). For each rabbit and anesthesia, mean systemic arterial pressure and heart rate were measured as carotid sinus pressure was changed in 10-mmHg steps between 40 and 150 mmHg. This set of measurements was repeated four times at 1-h intervals. A logistic function curve was fitted to the carotid sinus pressure-arterial pressure relationship. The parameters of this curve were then analyzed to delineate the specific effects of the anesthesias on the relationship. The main finding was that the response range and the slope parameters under alpha-chloralose anesthesia were significantly smaller than those obtained under the other anesthesias. Propylene glycol, used as the solvent for chloralose, did not affect the reflex control of arterial pressure or heart rate. The reflex under chloralose-urethan anesthesia showed characteristics similar to those under urethan anesthesia. We conclude that although alpha-chloralose has traditionally been used in the dog to obtain strong reflex responses, it weakens the reflex control of arterial pressure in the rabbit.

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.

PGE2 does not act at carotid sinus to raise arterial pressure in conscious sheep

1983 ◽  
Vol 245 (6) ◽  
pp. H1007-H1012
Author(s):  
B. A. Breuhaus ◽  
J. E. Chimoskey
Keyword(s):  
Carotid Artery ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Pressor Response ◽  
Direct Action ◽  
Peripheral Resistance ◽  
External Carotid Artery ◽  
External Carotid ◽  
Conscious Sheep ◽  
Female Sheep

Conscious chronically instrumented adult female sheep were used to determine whether direct action of prostaglandin E2 (PGE2) on the carotid sinus baroreceptors contributes to the pressor response observed during infusion of PGE2 into the common carotid artery (CCA). During infusion of PGE2 into the CCA caudal to an intact carotid sinus, into the CCA caudal to a denervated carotid sinus, and into the external carotid artery, mean arterial pressure (MAP) rose 17, 22, and 17 mmHg, respectively (P less than 0.01). Heart rate (HR) rose 6, 6, and 8 beats/min, respectively (P less than 0.05). Cardiac output (CO) was also measured by indicator dilution using indocyanine green. In these experiments with infusion of PGE2 into the external carotid artery, MAP rose 15 mmHg (P less than 0.01), HR increased 6 beats/min (P less than 0.05), CO did not change, and total peripheral resistance (TPR) increased 23% (P less than 0.01). With infusion of PGE2 past a denervated carotid sinus, MAP rose 20 mmHg (P less than 0.01), HR rose 4 beats/min (P less than 0.05), CO did not change, and TPR increased 29% (P less than 0.01). There were no statistically significant differences in MAP or HR responses when PGE2 was infused past an intact carotid sinus, past a denervated carotid sinus, or beyond the carotid sinus. There is no evidence that direct action of PGE2 on carotid sinus baroreceptors either augments or inhibits the observed pressor effect of intracarotid PGE2. Intracarotid PGE2 acts rostral to the carotid sinus to increase MAP, HR, and TPR in conscious sheep.

Carotid sinus control of pulsatile hemodynamics in halothane-anesthetized dogs

1980 ◽  
Vol 238 (3) ◽  
pp. H294-H299
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Open Loop ◽  
Hydraulic Power ◽  
Set Point ◽  
Hemodynamic Variables ◽  
Vascular Impedance ◽  
Mean Pressure ◽  
Anesthetized Dogs ◽  
Sinus Pressure

The open-loop characteristics of the carotid sinus baroreceptor reflex control of pulsatile arterial pressure-flow relations were studied in halothane-anesthetized dogs. Pressures and flows were measured in the ascending aorta, the celiac, mesenteric, renal, and iliac arteries and were used to compute values of regional vascular impedance and hydraulic power. The carotid sinuses were bilaterally isolated and perfused under conditions of controlled mean pressure with a constant sinusoidal component. Measurements were made with the vagi intact and after bilateral vagotomy. Maximum values of open-loop gain averaged -0.78 +/- 0.08 before and -1.42 +/- 0.20 after vagotomy. Vagotomy produced significant increases in the variation of all hemodynamic variables with carotid sinus pressure that were nonuniformly affected in the various regional vascular beds. Aortic and regional vascular impedance showed significant variations with carotid sinus pressure that were augmented by vagotomy. Aortic impedance exhibited a minimum at the normal set point. These results indicate that a) carotid sinus baroreflexes are well preserved with halothane anesthesia, b) thoracic baroreceptor-mediated reflexes exert significant hemodynamic effects on systemic hemodynamics around normal set point values of arterial pressure, c) systemic baroreceptors exert control over large as well as small vessel properties, and d) the baroreceptor-mediated reflexes produce significant influences on hydraulic power and its components.

Suppression of baroreceptor discharge by endothelin at high carotid sinus pressure

1992 ◽  
Vol 263 (1) ◽  
pp. R103-R108 ◽  
Author(s):  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Endothelial Cells ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
High Dose ◽  
Nerve Activity ◽  
Local Exposure ◽  
Potent Vasoconstrictor ◽  
Alpha Chloralose ◽  
Vasoconstrictor Peptide ◽  
Sinus Pressure

Endothelin is a potent vasoconstrictor peptide released from endothelial cells capable of producing marked and prolonged increases in arterial pressure. The purpose of this study was to determine whether endothelin alters the sensitivity of arterial baroreceptors. Multifiber baroreceptor activity was recorded from the vascularly isolated, endothelium-denuded carotid sinus in dogs anesthetized with alpha-chloralose. Local exposure of baroreceptors to endothelin at a concentration of 10(-8) M produced vasoconstriction of the carotid sinus as measured with sonomicrometer crystals but did not alter baroreceptor discharge significantly. A higher concentration of endothelin (10(-7) M) markedly suppressed baroreceptor activity, particularly at pressures greater than 100 mmHg (n = 7, P less than 0.05). The magnitude of the decrease in activity was dependent on the duration of exposure to endothelin. Baroreceptor activity measured at carotid pressures of 60, 100, and 200 mmHg averaged 23 +/- 4, 65 +/- 6, and 100 +/- 0% of maximum during control; 38 +/- 12, 61 +/- 9, and 74 +/- 15% after exposure to endothelin (10(-7) M) for 2 min; and 27 +/- 8, 53 +/- 12, and 56 +/- 19% after 12 min, respectively. The suppression of nerve activity with the high dose of endothelin was not accompanied by additional vasoconstriction, suggesting a direct effect of endothelin on nerve endings. We speculate that endothelin released from endothelial cells may act in a paracrine manner to suppress activity of baroreceptors, particularly at high levels of arterial pressure. Such an action would interfere with the buffering capacity of the baroreflex and promote hypertension.

Comparison of carotid sinus baroreceptors in dogs, cats, monkeys, and rabbits

1984 ◽  
Vol 247 (1) ◽  
pp. R52-R56
Author(s):  
J. P. Gilmore ◽  
E. Tomomatsu
Keyword(s):  
Arterial Pressure ◽  
Single Unit ◽  
Static Pressure ◽  
Carotid Sinus ◽  
Lower Threshold ◽  
Threshold Pressure ◽  
Experimental Conditions ◽  
Single Unit Recordings ◽  
Sinus Pressure

Single-unit recordings were obtained from the vascularly isolated Krebs-Henseleit-perfused carotid sinus of the rabbit and cat, and the results were compared with those obtained previously from the monkey and dog. Carotid sinus pressure was altered using static pressure steps. There was a highly significant correlation between resting arterial pressure and carotid sinus baroreceptor threshold pressure. The baroreceptors of the monkey and rabbit had a significantly lower threshold than those of the dog and cat. The baroreceptors of the monkey had a significantly lower gain than those of the three nonprimates. This is the first study in which baroreceptor activity has been studied under the same experimental conditions in four different species.

Baroreceptor-mediated compensation for hemodynamic effects of positive end-expiratory pressure

1999 ◽  
Vol 86 (1) ◽  
pp. 285-293 ◽  
Author(s):  
Stephen S. Blevins ◽  
Martha J. Connolly ◽  
Drew E. Carlson
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Baroreceptor Reflex ◽  
Right Atrial ◽  
Positive End Expiratory Pressure ◽  
Carotid Baroreceptor ◽  
The Right

The roles of the carotid arterial baroreceptor reflex and of vagally mediated mechanisms during positive end-expiratory pressure (PEEP) were determined in pentobarbital-anesthetized dogs with isolated carotid sinuses. Spontaneously breathing dogs were placed on PEEP (5–10 cmH2O) with the carotid sinus pressure set to the systemic arterial pressure (with feedback) or to a constant pressure (no feedback). Right atrial volume was measured with a conductance catheter. With carotid baroreceptor feedback before bilateral cervical vagotomy, total peripheral resistance increased ( P < 0.01) and mean arterial pressure decreased (−9.8 ± 4.3 mmHg) in response to PEEP. With no feedback after vagotomy, mean arterial pressure decreased to a greater extent (−45 ± 6 mmHg, P < 0.01), and total peripheral resistance decreased ( P < 0.05) in response to PEEP. In contrast, cardiac index decreased similarly during PEEP ( P < 0.01) for all baroreceptor and vagal inputs. This response comprised a decrease in the passive phase of right ventricular filling ( P< 0.01) that was not matched by the estimated increase in active right atrial output. Although the carotid baroreceptor reflex and vagally mediated mechanisms elicit vasoconstriction to compensate for the effects of PEEP on the arterial pressure, these processes fail to defend cardiac output because of the profound effect of PEEP on the passive filling of the right ventricle.

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