scholarly journals Effects of calcium channel antagonists on carotid sinus baroreflex control of arterial pressure and heart rate in anesthetized dogs.

1989 ◽  
Vol 64 (2) ◽  
pp. 276-286 ◽  
Author(s):  
D F Rigel ◽  
R W Millard
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Calcium Channel ◽  
Carotid Sinus ◽  
Calcium Channel Antagonists ◽  
Baroreflex Control ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs

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 At each interval of CSP, blood was withdrawn for AVP analysis by radioimmunoassay.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.

Rapid resetting of baroreflexes in hypertensive dogs

1992 ◽  
Vol 262 (5) ◽  
pp. H1508-H1514
Author(s):  
M. J. Brunner ◽  
M. D. Kligman
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Experimental Hypertension ◽  
Arterial Baroreflex ◽  
Short Term ◽  
Baroreflex Control ◽  
Pentobarbital Sodium ◽  
Reflex Gain ◽  
Pentobarbital Sodium Anesthesia

The hypothesis tested was that the rapid resetting of the arterial baroreflex control of arterial pressure in normotension could be demonstrated in experimental hypertension. After the development of experimental hypertension (using a bilateral renal wrap technique), rapid resetting of arterial pressure and heart rate (HR) was acutely assessed under pentobarbital sodium anesthesia in hypertensive and normotensive vagotomized dogs. The carotid sinus area was isolated and perfused at controlled carotid sinus pressures (CSPs). Baroreflex response [mean arterial pressure (MAP) and HR] curves were measured after three carotid sinus conditioning pressures (50, 125, and 200 mmHg) were applied. For the MAP response, the CSPo (CSP at point of maximum reflex gain) increased significantly to the same extent in both groups with increasing conditioning pressures (with 22.2 and 16.7% resetting in the normotensive group, and 20.3 and 14.2% resetting in the hypertensive group). We conclude that short-term adjustments to changes in prevailing pressure (rapid resetting) occur in the arterial pressure response in experimental hypertension to the same extent seen in normotension.

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.

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.

Baroreflex control of arterial and venous compliances and vascular capacity in hypertensive dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H96-H102 ◽  
Author(s):  
G. G. Bishop ◽  
K. Shigemi ◽  
J. P. Freeman ◽  
M. J. Brunner
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Arterial Compliance ◽  
Characteristic Curve ◽  
Venous Blood ◽  
Baroreflex Control ◽  
Reservoir Volume ◽  
Carotid Sinus Baroreflex ◽  
Pentobarbital Sodium Anesthesia ◽  
Venous Blood Volume

The ability of the carotid sinus baroreflex to elicit reflex changes in vascular capacity was studied in chronically hypertensive (one-kidney, one-clip) and sham-operated normotensive dogs under pentobarbital sodium anesthesia. Vascular compliances and reflex-induced changes in external reservoir volume were measured in response to changes in isolated carotid sinus pressure (CSP). The mean arterial pressure-CSP reflex characteristic curve was shifted to a higher arterial pressure with hypertension with no change in maximum reflex gains. Arterial compliance in both groups increased significantly (P < 0.01) when CSP was increased from 50 to 200 mmHg. Total, arterial, and venous vascular compliances were not different in normotensive and hypertensive groups. Changes in CSP caused no significant changes in either total systemic vascular or calculated venous compliances. A decrease in CSP from 250 to 50 mmHg resulted in an increase in external reservoir volume of 8.02 +/- 1.03 and 7.44 +/- 1.33 ml/kg in normotensive and hypertensive groups, respectively, with changes in venous volume of 11.99 +/- 1.39 and 12.58 +/- 1.52 ml/kg (NS). We conclude that despite the increase in arterial resistance, Goldblatt hypertensive dogs retain the ability to make short-term reflex adjustments in both arterial pressure and venous blood volume.

Arterial pressure-flow relationships in hypertensive dogs: effect of carotid sinus baroreflex

1993 ◽  
Vol 265 (3) ◽  
pp. H986-H992
Author(s):  
M. J. Brunner ◽  
G. G. Bishop ◽  
K. Shigemi ◽  
J. P. Freeman ◽  
D. Chung
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Coefficient Of Determination ◽  
Experimental Hypertension ◽  
Baroreflex Control ◽  
Pressure Flow ◽  
Hypertensive Group ◽  
Carotid Sinus Baroreflex ◽  
Reflex Gain

The effect of the carotid sinus baroreflex reflex on arterial pressure-flow relationships was studied in Goldblatt hypertensive and normotensive dogs on cardiopulmonary bypass. Dogs were anesthetized with pentobarbital sodium, vagotomized, and the carotid sinuses were isolated at controlled carotid sinus pressures (CSP). The mean arterial pressure-flow relationships were measured at different levels of CSP. The arterial pressure-flow relationship was found to be linear except at extreme levels of flow. The slopes derived from the linear regression of the pressure-flow relationships [total peripheral resistance (TPR)] were 1.466 +/- 0.111 and 0.786 +/- 0.13 mmHg.ml-1 x min.kg at CSP of 50 and 200 mmHg in the normotensive group and 1.758 +/- 0.183 and 0.937 +/- 0.114 mmHg.ml-1 x min.kg at CSP of 50 and 250 mmHg in the hypertensive group. The increases in slope measured when CSP was decreased from saturation to threshold were 0.68 mmHg.ml-1 x min.kg (187% increase) in the normotensive group and 0.82 mmHg.ml-1 x min.kg (188% increase) in the hypertensive group. Zero-flow arterial pressures at CSP of 50, 125, and 200 mmHg were found to be 23.1 +/- 2.9, 21.7 +/- 2.2, and 17.1 +/- 1.8 mmHg in the normotensive group and 28.4 +/- 2.2, 23.8 +/- 1.5, and 20.0 +/- 1.2 mmHg in the hypertensive group. A nonlinear model fit was found to give a significantly better fit [coefficient of determination (r2) = 0.932 linear, 0.956 nonlinear] of the arterial pressure-flow relationships. We conclude that, in experimental hypertension, carotid baroreflex control of TPR is shifted to a higher operating point without any reduction in overall reflex gain.

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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