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.

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.

Chronic isolation of carotid sinus baroreceptor region in conscious normotensive and hypertensive rats

1998 ◽  
Vol 275 (1) ◽  
pp. H322-H329 ◽  
Author(s):  
Kelly P. McKeown ◽  
Artin A. Shoukas
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Conscious Rat ◽  
Sd Rats ◽  
The Right ◽  
Reflex System

We have developed a chronic technique to isolate the carotid sinus baroreceptor region in the conscious rat model. Our technique, when used in conjunction with other methods, allows for the study of the control of arterial pressure, heart rate, and cardiac output by the carotid sinus baroreceptor reflex in conscious, unrestrained rats. The performance of our technique was evaluated in two strains: normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Each rat was instrumented with an aortic flow probe and a catheter placed in the right femoral artery to monitor cardiac output and arterial pressure, respectively. The cervical sympathetic trunk and aortic depressor nerve were ligated and cut bilaterally, leaving vagus nerves intact. The right and left carotid sinuses were isolated using our new technique. We tested the open-loop function of the carotid sinus baroreceptor reflex system in the conscious rat after recovery from the isolation surgery. We found that changes in nonpulsatile carotid sinus pressure caused significant changes in arterial pressure, heart rate, and total peripheral resistance in both rat strains. However, the cardiac output responses differed dramatically between strains. Significant changes were seen in the cardiac output response of SHR, whereas no significant changes were observed in normotensive SD rats. We have found this technique to be a highly reliable tool for the study of the carotid sinus baroreceptor reflex system in the conscious rat.

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.

Effect of carotid or aortic baroreceptor denervation on arterial pressure during hemorrhage in conscious dogs

2001 ◽  
Vol 280 (6) ◽  
pp. R1642-R1649 ◽  
Author(s):  
Terry N. Thrasher ◽  
Cassandra Shifflett
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Conscious Dogs ◽  
Carotid Baroreceptors ◽  
Intact Condition ◽  
Aortic Baroreceptors

We studied the effect of chronically denervating aortic baroreceptors (ABR; n = 6) or carotid baroreceptors (CBR; n= 7) on mean arterial pressure (MAP) and heart rate (HR) responses to hemorrhage in the dog. Neither denervation had a significant effect on basal MAP, the variability (standard deviation) of MAP, or resting HR. However, the breakpoint of MAP (defined as the volume of blood removed when MAP fell more than 10% below control and declined monotonically thereafter) was significantly reduced in dogs with only ABR functional (12.4 ± 1.4 ml/kg) compared with the volume in the intact condition (18.9 ± 1.8 ml/kg). In contrast, there was no difference in the breakpoint or the MAP at any time during hemorrhage in dogs with both CBR functional compared with their intact responses. In a different group of dogs ( n = 6), responses were determined with both CBR operating and again after unilateral denervation, leaving only one CBR (1CBR) functional. Basal MAP and the variability of MAP were not altered in dogs with only 1CBR functional, but the breakpoint (11.7 ± 1.4 ml/kg) during hemorrhage was significantly different compared with responses with two CBR (21.2 ± 2.3 ml/kg), and MAP fell to much lower levels. These results indicate that the CBR can compensate fully for loss of ABR during hemorrhage but not vice versa; and bilateral CBR inputs are required for normal responses to hemorrhage.

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.

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.

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.

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.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

Sign in / Sign up

Export Citation Format

Share Document