Comparison of carotid baroreflex control of plasma AVP concentration in conscious and anesthetized dogs

1991 ◽  
Vol 261 (4) ◽  
pp. R950-R956 ◽  
Author(s):  
K. E. Wehberg ◽  
G. J. Gala ◽  
M. J. Brunner
Keyword(s):  
Heart Rate ◽  
Carotid Sinus ◽  
Normal Component ◽  
Vagal Afferents ◽  
Baroreflex Control ◽  
Carotid Baroreflex ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs ◽  
Plasma Arginine ◽  
Sinus Pressure

We compared carotid sinus baroreflex control of endogenous plasma arginine vasopressin (AVP) in chronically prepared conscious and acutely prepared anesthetized dogs. The carotid sinuses of both conscious and pentobarbital-anesthetized dogs were isolated bilaterally and perfused at constant pressures. Carotid sinus pressure (CSP) was changed between 200 and 50 mmHg in 25-mmHg steps in intact conscious and anesthetized dogs. Similar runs were repeated after vagotomy. Mean arterial pressure (MAP) and heart rate (HR) were monitored. At each interval of CSP, blood was withdrawn for AVP analysis by radioimmunoassay. MAP responses to changes in CSP were not different in the four experimental groups. Both anesthesia and vagotomy increased the HR responses to changes in CSP. With vagi intact, AVP increased at high CSP in conscious but not in anesthetized dogs. After vagotomy, low CSP led to an increase in plasma AVP that did not differ between conscious and anesthetized dogs. The results suggest that the release of AVP is modulated by the action of the carotid baroreflex as a normal component of an integrated efferent response. The response is similar in conscious and pentobarbital-anesthetized dogs and is normally buffered by reflexes with vagal afferents.

Carotid baroreflex control of heart rate and blood pressure during ES leg cycling in paraplegics

2000 ◽  
Vol 88 (3) ◽  
pp. 957-965 ◽  
Author(s):  
Jacqui Raymond ◽  
Glen M. Davis ◽  
Martinus N. van der Plas ◽  
Herbert Groeller ◽  
Scott Simcox
Keyword(s):  
Heart Rate ◽  
Carotid Sinus ◽  
Baroreflex Control ◽  
Cycling Exercise ◽  
Rightward Shift ◽  
Spinal Lesions ◽  
Carotid Baroreflex ◽  
Carotid Sinus Baroreflex ◽  
Leg Cycling ◽  
Sinus Pressure

This study investigated control of heart rate (HR) and mean arterial pressure (MAP) at rest and during electrical stimulation (ES) leg cycling exercise (LCE) in paraplegics (Para). Seven men with complete spinal lesions (T5–T11) and six able-bodied (AB) men participated in this study. Beat-to-beat changes in HR and MAP were recorded during carotid sinus perturbation. Carotid baroreflex function curves were derived at rest and during ES-LCE for Para and during voluntary cycling (Vol) for AB. From rest to ES-LCE, oxygen uptake (V˙o 2) increased (by 0.43 l/min) and HR rose (by 11 beats/min), yet MAP remained unchanged. In AB, Vol increased V˙o 2 (by 0.53 l/min), HR (by 22 beats/min), and MAP (by 8 mmHg). ES-LCE did not alter the carotid sinus pressure (CSP)-MAP relationship, but it displaced the CSP-HR relationship upward relative to rest. No rightward shift was observed during ES-LCE. Vol by AB produced an upward and rightward displacement of the CSP-MAP and CSP-HR relationships relative to rest. These findings suggested that the carotid sinus baroreflex was not reset during ES-LCE in Para.

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.

Carotid baroreflex control during hemorrhage in conscious and anesthetized dogs

1993 ◽  
Vol 265 (1) ◽  
pp. R195-R202 ◽  
Author(s):  
B. P. Geerdes ◽  
K. L. Frederick ◽  
M. J. Brunner
Keyword(s):  
Carotid Sinus ◽  
Characteristic Curve ◽  
Control Level ◽  
Peripheral Resistance ◽  
Baroreflex Control ◽  
Carotid Baroreflex ◽  
Reflex Gain ◽  
Anesthetized Dogs ◽  
Plasma Arginine ◽  
Sinus Pressure

The hypothesis was tested that carotid baroreflex gain is increased after 20% hemorrhage. The baroreceptor reflex responses to changes in carotid sinus pressure (CSP) were measured in control, 20% hemorrhage, and reinfusion conditions in three experimental groups: conscious intact (n = 7), anesthetized intact (n = 8), and anesthetized vagotomized (n = 8) dogs. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), and calculated total peripheral resistance (TPR) responses to changes in CSP were measured. At any given CSP, MAP, CO, and SV all decreased significantly with the 20% hemorrhage, as reflected by a downward shift in the reflex characteristic curve with no change in overall reflex range or gain. In contrast, TPR and HR responses to CSP were not significantly altered by 20% hemorrhage; reflex curves and gains were comparable to control conditions. In the conscious intact dogs, the maximal reflex gain, Gmax, for the MAP response was -1.365 +/- 0.25, -1.298 +/- 0.33, and -1.324 +/- 0.25 in control, 20% hemorrhage, and reinfusion conditions, respectively, and was not significantly altered by hemorrhage. In the same group, the Gmax for the HR response was -1.792 +/- 0.65, -1.709 +/- 0.33, and -1.986 +/- 0.67 in control, 20% hemorrhage, and reinfusion conditions, respectively; baroreflex gain on HR was not increased with hemorrhage. Plasma arginine vasopressin (AVP), an increase in which has been proposed to augment baroreflex gain, increased from a control level of 0.98 +/- 0.27 to 9.66 +/- 2.67 pg/ml during 20% hemorrhage in the conscious intact dogs; despite the increase in plasma AVP during hemorrhage, augmentation of baroreflex gain was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in canine cardiac function and venous return curves by the carotid baroreflex

1986 ◽  
Vol 251 (2) ◽  
pp. H288-H296 ◽  
Author(s):  
A. S. Greene ◽  
A. A. Shoukas
Keyword(s):  
Arterial Pressure ◽  
Cardiac Function ◽  
Venous Return ◽  
Carotid Sinus ◽  
Baroreceptor Reflex ◽  
Primary Mechanism ◽  
Carotid Baroreflex ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs ◽  
Sinus Pressure

Venous return curves and cardiac function relationships were simultaneously determined in 10 pentobarbital-anesthetized dogs at three different isolated carotid sinus pressures. Changing carotid sinus pressure (CSP) between 50 and 200 mmHg produced large changes in the zero flow intercept of the venous return curves from 15.37 +/- 0.97 to 11.94 +/- 1.36 mmHg (P less than 0.001) but no change in slope. These changes in the intercept of the venous return curve were due to alterations in systemic vascular capacity caused by the carotid sinus baroreceptor reflex. Changes in the cardiac function curve with baroreceptor pressure were masked by concomitant changes in arterial pressure afterload; however, when arterial pressure was controlled, there was a significant change in the slope of the cardiac function curve from 60.32 +/- 26.9 to 37.06 +/- 13.31 ml X min-1 X kg-1 X mmHg-1 as CSP was changed from 50 to 200 mmHg. We conclude that changes in vascular capacity are the primary mechanism responsible for changes in cardiac output during activation of the carotid sinus baroreflex.

Interaction of right and left carotid sinus baroreflexes in the dog

1986 ◽  
Vol 250 (1) ◽  
pp. H96-H107 ◽  
Author(s):  
A. S. Greene ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Heart Rate ◽  
Tidal Volume ◽  
Carotid Sinus ◽  
The Other ◽  
Reflex Response ◽  
Pentobarbital Sodium ◽  
Simultaneous Excitation ◽  
Carotid Sinus Baroreflex ◽  
The Right ◽  
Sinus Pressure

Carotid sinus reflex interactions were studied in 10 dogs anesthetized with pentobarbital sodium. The right and left carotid sinus regions were isolated and perfused at controlled pressures. Pressure in the right and left carotid sinuses were independently varied, and the resulting steady-state reflex changes in arterial pressure, heart rate, respiratory frequency, tidal volume, and total ventilation were measured. Reflex changes when carotid sinus pressure was changed on one side were strongly influenced by pressure in the contralateral carotid sinus (P less than 0.05). Right carotid sinus gain was found to be 0.628 +/- 0.058 at a left carotid sinus pressure of 50 mmHg and 0.148 +/- 0.027 when left carotid sinus pressure was 200 mmHg. Similar results were found for left carotid sinus gain. Suppression was also found for heart rate, respiratory rate, tidal volume, and total ventilation. The hypothesis that rapid resetting of one carotid sinus baroreflex might influence responses from the other side was also tested. Although ipsilateral resetting was consistently observed, no contralateral component of the resetting was detected. An additional inhibitory summation between the right and left carotid sinuses was found such that simultaneous excitation of both receptors resulted in a smaller reflex response than did the sum of individual responses. Sympathetic denervation of the carotid sinus region had no effect.

Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H815-H822 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Cervical Vagotomy ◽  
Curve Upward ◽  
Sinus Pressure

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.

Response of arterial resistance and critical pressure to changes in perfusion pressure in canine hindlimb

1993 ◽  
Vol 265 (6) ◽  
pp. H1939-H1945 ◽  
Author(s):  
I. Shrier ◽  
S. Magder
Keyword(s):  
Critical Pressure ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Dynamic Pressure ◽  
Arterial Resistance ◽  
Carotid Baroreflex ◽  
Anesthetized Dogs ◽  
Flow Mediated Vasodilation ◽  
Central Factors ◽  
Sinus Pressure

The dynamic pressure-flow relationship in the canine hindlimb at normal arterial pressure is best explained by modeling a Starling resistor (critical pressure, Pcrit) at the level of the arterioles. Regulation of flow can therefore occur at the Starling resistor through changes in Pcrit or along the length of the vessel through changes in arterial resistance (Ra). We hypothesized that increasing perfusion pressure (Pper) would increase Pcrit due to the myogenic response but would decrease Ra because of flow-mediated vasodilation and passive effects. We pump-perfused vascularly isolated hindlimbs of anesthetized dogs and then measured Pcrit and calculated Ra over Pper range of 75-175 mmHg. When Pper was increased from 75 to 175 mmHg, Pcrit increased from 33 +/- 2 to 48 +/- 6 (means +/- SE) mmHg, whereas Ra decreased from 10.1 +/- 1.2 to 7.86 +/- 0.7 mmHg.min.100 g.ml-1 (P < 0.01). Thus the responses of Pcrit and Ra to an increase in Pper were dissociated. In a second part of the study, we lowered carotid sinus pressure to determine the effects of central factors on local autoregulation. A decrease in carotid sinus pressure increased Pcrit and Ra at each Pper (P < 0.05). We conclude that an increase in Pper causes the arterial vasculature to constrict at the level of the Starling resistor and dilate more proximally. The carotid baroreflex causes an increase in tone throughout the arterial vasculature but does not alter the local response to increases in Pper.

Hemodynamic and respiratory responses to carotid sinus pressure alteration in experimental hypertension

1993 ◽  
Vol 74 (3) ◽  
pp. 1274-1279 ◽  
Author(s):  
M. J. Brunner ◽  
M. D. Kligman
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Experimental Hypertension ◽  
Baroreflex Control ◽  
Hypertensive Group ◽  
The Mean ◽  
Respiratory Responses ◽  
Sinus Pressure

The purpose of this study was to determine whether baroreflex control of respiratory responses is diminished in hypertension. Ten dogs were made chronically hypertensive with use of a bilateral renal wrap technique. Eight sham-operated dogs served as normotensive controls. After the development of experimental hypertension, carotid baroreflex control of arterial pressure, heart rate, respiratory frequency, tidal volume, and ventilation was acutely assessed. Under pentobarbital anesthesia and with bilateral vagotomy, the carotid sinuses were isolated and perfused at controlled pressures. Before the carotid sinus region was manipulated, the mean arterial pressure was significantly higher (P < 0.005) in the hypertensive group (146.4 +/- 2.3 mmHg) than in the normotensive group (124.7 +/- 2.6 mmHg). The mean arterial pressures and heart rates measured at every level of carotid sinus pressure were significantly higher in the hypertensive group. Reflex gain of heart rate, but not mean arterial pressure, was significantly reduced in the hypertensive group. Respiratory frequency, tidal volume, and ventilatory responses to changes in carotid sinus pressure were significant and resulted in an approximately 40% reflex change in ventilation. These responses were not diminished in the hypertensive group. We conclude that respiratory baroreflex responses are preserved in experimental hypertension.

Effects of fentanyl on carotid sinus baroreflex control of circulation in rabbits

1989 ◽  
Vol 256 (3) ◽  
pp. R625-R631
Author(s):  
H. Ohsumi ◽  
M. Sakamoto ◽  
T. Yamazaki ◽  
F. Okumura
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Conscious State ◽  
Hemodynamic Responses ◽  
Baroreflex Control ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Carotid Sinus Baroreflex

The effects of intravenous administration of fentanyl on carotid sinus baroreflex control of hemodynamics were investigated in chronically instrumented rabbits. Carotid sinus baroreflex was assessed by bilateral carotid occlusion (BCO), and the responses of mean arterial pressure (MAP), heart rate (HR), mean ascending aortic flow (MAF), and total peripheral resistance (TPR) were obtained. Hemodynamic responses to BCO were examined with cumulative doses of 5, 10, and 15 micrograms/kg of fentanyl. Fentanyl did not affect MAP and TPR but reduced HR and MAF dose dependently. Fentanyl did not attenuate the MAP response to BCO significantly. In contrast, fentanyl significantly attenuated the TPR response from 0.126 +/- 0.003 to 0.104 +/- 0.005 mmHg.min-1.ml-1 and augmented the HR response from 31 +/- 2 to 47 +/- 3 beats/min in the conscious state and at 15 micrograms/kg of fentanyl, respectively. The administration of atropine after the fentanyl attenuated MAP and HR responses to 79.9 and 27.7% of those of 10 micrograms/kg of fentanyl, respectively. We suggest that these dissociated hemodynamic responses reflect the vagotonic and sympatholytic effects of fentanyl on the baroreflex pathways.

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