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.

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.

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.

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.

scholarly journals Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Afferents ◽  
Baroreflex Control ◽  
Group Iii ◽  
Carotid Baroreflex

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.

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.

scholarly journals Noninvasive calculation of the aortic blood pressure waveform from the flow velocity waveform: a proof of concept

2015 ◽  
Vol 309 (5) ◽  
pp. H969-H976 ◽  
Author(s):  
Samuel Vennin ◽  
Alexia Mayer ◽  
Ye Li ◽  
Henry Fok ◽  
Brian Clapp ◽  
...  
Keyword(s):  
Experimental Data ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Flow Velocity ◽  
Aortic Pressure ◽  
Pressure Waveform ◽  
Arterial Tree ◽  
Measured Flow ◽  
Rms Error ◽  
Measured Pressure

Estimation of aortic and left ventricular (LV) pressure usually requires measurements that are difficult to acquire during the imaging required to obtain concurrent LV dimensions essential for determination of LV mechanical properties. We describe a novel method for deriving aortic pressure from the aortic flow velocity. The target pressure waveform is divided into an early systolic upstroke, determined by the water hammer equation, and a diastolic decay equal to that in the peripheral arterial tree, interposed by a late systolic portion described by a second-order polynomial constrained by conditions of continuity and conservation of mean arterial pressure. Pulse wave velocity (PWV, which can be obtained through imaging), mean arterial pressure, diastolic pressure, and diastolic decay are required inputs for the algorithm. The algorithm was tested using 1) pressure data derived theoretically from prespecified flow waveforms and properties of the arterial tree using a single-tube 1-D model of the arterial tree, and 2) experimental data acquired from a pressure/Doppler flow velocity transducer placed in the ascending aorta in 18 patients (mean ± SD: age 63 ± 11 yr, aortic BP 136 ± 23/73 ± 13 mmHg) at the time of cardiac catheterization. For experimental data, PWV was calculated from measured pressures/flows, and mean and diastolic pressures and diastolic decay were taken from measured pressure (i.e., were assumed to be known). Pressure reconstructed from measured flow agreed well with theoretical pressure: mean ± SD root mean square (RMS) error 0.7 ± 0.1 mmHg. Similarly, for experimental data, pressure reconstructed from measured flow agreed well with measured pressure (mean RMS error 2.4 ± 1.0 mmHg). First systolic shoulder and systolic peak pressures were also accurately rendered (mean ± SD difference 1.4 ± 2.0 mmHg for peak systolic pressure). This is the first noninvasive derivation of aortic pressure based on fluid dynamics (flow and wave speed) in the aorta itself.

scholarly journals Carotid baroreflex control of heart rate is enhanced, while control of mean arterial pressure is preserved during whole body heat stress in young healthy men

2016 ◽  
Vol 311 (4) ◽  
pp. R735-R741 ◽  
Author(s):  
Davor Krnjajic ◽  
Dustin R. Allen ◽  
Cory L. Butts ◽  
David M. Keller
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Whole Body ◽  
Chamber Pressure ◽  
Carotid Baroreflex ◽  
Whole Body Heat Stress ◽  
Neck Pressure ◽  
Body Heat

Whole body heat stress (WBH) results in numerous cardiovascular alterations that ultimately reduce orthostatic tolerance. While impaired carotid baroreflex (CBR) function during WBH has been reported as a potential reason for this decrement, study design considerations may limit interpretation of previous findings. We sought to test the hypothesis that CBR function is unaltered during WBH. CBR function was assessed in 10 healthy male subjects (age: 26 ± 3; height: 185 ± 7 cm; weight: 82 ± 10 kg; BMI: 24 ± 3 kg/m2; means ± SD) using 5-s trials of neck pressure (+45, +30, and +15 Torr) and neck suction (−20, −40, −60, and −80 Torr) during normothermia (NT) and passive WBH (Δ core temp ∼1°C). Analyses of stimulus response curves (four-parameter logistic model) for CBR control of heart rate (CBR-HR) and mean arterial pressure (CBR-MAP), as well as separate two-way ANOVA of the hypotensive and hypertensive stimuli (factor 1: thermal condition, factor 2: chamber pressure), were performed. For CBR-HR, maximal gain was increased during WBH (−0.73 ± 0.11) compared with NT (−0.39 ± 0.04, mean ± SE, P = 0.03). In addition, the CBR-HR responding range was increased during WBH (33 ± 5) compared with NT (19 ± 2 bpm, P = 0.03). Separate analysis of hypertensive stimulation revealed enhanced HR responses during WBH at −40, −60, and −80 Torr (condition × chamber pressure interaction, P = 0.049) compared with NT. For CBR-MAP, both logistic analysis and separate two-way ANOVA revealed no differences during WBH. Therefore, in response to passive WBH, CBR control of heart rate (enhanced) and arterial pressure (no change) is well preserved.

scholarly journals Mean Blood Pressure and Velocity for Calculation of Ventricular Systolic Work

1998 ◽  
Vol 41 (1) ◽  
pp. 27-28
Author(s):  
Milan Valach
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diastolic Pressure ◽  
Weighted Average ◽  
Average Pressure ◽  
Mean Pressure ◽  
The Mean ◽  
Definition Of ◽  
Ejection Phase

In physiology, the mean arterial pressure is defined as an average pressure during one or several cardiac cycles. When calculus is not used, the mean pressure is approximately calculated as the diastolic pressure plus one third of the pulse pressure. In this article it is demonstrated that, when ventricular systolic work is concerned, the above definition of mean pressure must be replaced by a weighted average during the ejection phase of the systole. This gives a formula, by which a much higher estimate of the mean pressure is obtained.

Sign in / Sign up

Export Citation Format

Share Document