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.

scholarly journals Changes in vascular properties, not ventricular properties, predominantly contribute to baroreflex regulation of arterial pressure

2015 ◽  
Vol 308 (1) ◽  
pp. H49-H58 ◽  
Author(s):  
Takafumi Sakamoto ◽  
Takamori Kakino ◽  
Kazuo Sakamoto ◽  
Tomoyuki Tobushi ◽  
Atsushi Tanaka ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Arterial Pressure ◽  
Venous Return ◽  
Transfer Functions ◽  
Carotid Sinus ◽  
Left Ventricular ◽  
Sensitivity Analyses ◽  
Data Set ◽  
Anesthetized Dogs ◽  
Sinus Pressure

Baroreflex modulates both the ventricular and vascular properties and stabilizes arterial pressure (AP). However, how changes in those mechanical properties quantitatively impact the dynamic AP regulation remains unknown. We developed a framework of circulatory equilibrium, in which both venous return and cardiac output are expressed as functions of left ventricular (LV) end-systolic elastance (Ees), heart rate (HR), systemic vascular resistance (R), and stressed blood volume (V). We investigated the contribution of each mechanical property using the framework of circulatory equilibrium. In six anesthetized dogs, we vascularly isolated carotid sinuses and randomly changed carotid sinus pressure (CSP), while measuring the LV Ees, aortic flow, right and left atrial pressure, and AP for at least 60 min. We estimated transfer functions from CSP to Ees, HR, R, and V in each dog. We then predicted these parameters in response to changes in CSP from the transfer functions using a data set not used for identifying transfer functions and predicted changes in AP using the equilibrium framework. Predicted APs matched reasonably well with those measured ( r2 = 0.85–0.96, P < 0.001). Sensitivity analyses indicated that Ees and HR (ventricular properties) accounted for 14 ± 4 and 4 ± 2%, respectively, whereas R and V (vascular properties) accounted for 32 ± 4 and 39 ± 4%, respectively, of baroreflex-induced AP regulation. We concluded that baroreflex-induced dynamic AP changes can be accurately predicted by the transfer functions from CSP to mechanical properties using our framework of circulatory equilibrium. Changes in the vascular properties, not the ventricular properties, predominantly determine baroreflex-induced AP regulation.

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 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.

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.

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 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)

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.

Interaction between carotid and cardiopulmonary baroreflexes in control of plasma ADH

1981 ◽  
Vol 241 (3) ◽  
pp. H431-H434 ◽  
Author(s):  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Superior Vena ◽  
Vena Cava ◽  
Vagal Afferents ◽  
Plasma Vasopressin ◽  
Anesthetized Dogs ◽  
Cardiopulmonary Receptors ◽  
Induced Changes ◽  
Sinus Pressure

The purpose of this study was to determine if there is an interaction between carotid baroreceptors (CBR) and cardiopulmonary receptors with vagal afferents (CPVA) in the control of plasma vasopressin (ADH). Changes in ADH (radioimmunoassay) in the superior vena cava were determined in 13 chloralose-anesthetized dogs with aortic nerves sectioned during concomitantly induced changes in CBR and CPVA input. CBR input was changed by altering pressure (CSP) in the isolated perfused sinuses. Carotid sinus pressure (CSP) was initially set at 50 mmHg. The CPVA input was reversibly interrupted by cooling the vagi to 0 degrees C while CSP was concomitantly increased to 135 or 200 mmHg or was held constant at 50 mmHg. Vagal cold block (VCB) with CSP held constant at 50 mmHg resulted in large increases in arterial pressure and plasma vasopressin. Increases in CSP to 200 mmHg resulted in significant decreases in arterial pressure and in plasma vasopressin despite concomitant VCB. VCB and concomitant increase in CSP to 135 mmHg resulted in a significant fall in arterial pressure, whereas plasma vasopressin tended to increase. Thus, the influence on arterial pressure of raising CSP to 135 mmHg exceeds that of VCB. In contrast, the influence of VCB on ADH equals or exceeds that of raising CSP to 135 mmHg. These differential responses of arterial pressure and plasma ADH suggest an interaction between CBR and CPVA in the control of ADH and arterial pressure.

Enhanced carotid sinus baroreflex responses in dogs with chronic A-V block

1975 ◽  
Vol 38 (1) ◽  
pp. 1-4 ◽  
Author(s):  
J. DiSalvo ◽  
R. Reynolds ◽  
J. L. Robinson ◽  
G. Grupp
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Ventricular Rate ◽  
Vagus Nerves ◽  
Atrial Rate ◽  
Carotid Sinus Baroreflex ◽  
Sinus Pressure

Effects of carotid sinus pressure on arterial pressure, atrial rate, and ventricular rate were examined in anesthetized normal dogs and in dogs with chronic complete A-V block. Change in arterial pressure per mmHg change in sinus pressure was 0.8 plus or minus 0.2 mmHg for controls but increased (P is less than 0.001) to 1.6 plus or minus 0.1 mmHg in A-V blocked dogs. Arterial pressure was 140–145 mmHg at low sinus pressure in both groups, but at high sinus pressure arterial pressure was significantly lower in A-V blocked dogs (44 plus or minus 4 mmHg) than in controls (92 plus or minus 8 mmHg). These differences were virtually abolished after vagotomy. Heart rate increased in normal dogs as sinus pressure was increased before vagotomy, but decreased after vagotomy. In blocked dogs atrial and ventricular rates decreased at high sinus pressure either before or after vagotomy. The results show that reflex circulatory responses to changes in carotid sinus pressure are enhanced in dogs with A-V block. This enhancement may involve attenuation of buffering influences exerted from other baroreceptors whose afferents are in the vagus nerves.

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